Reaching Adolescent Gay,Bisexual, and Queer Men Online: Development and Refinement of a National Recruitment Strategy

BackgroundUsing social networking websites to recruit research participants is increasingly documented in the literature, although few studies have leveraged these sites to reach those younger than 18 years.ObjectiveTo discuss the development and refinement of a recruitment protocol to reach and engage adolescent gay, bisexual, and other teenaged men who have sex with men (AGBM). Participants were recruited for development and evaluation activities related to Guy2Guy, a text messaging–based human immunodeficiency virus infection prevention program.MethodsEligibility criteria included being between 14 to 18 years old; being a cisgender male; self-identifying as gay, bisexual, and/or queer; being literate in English, exclusively owning a cell phone, enrolled in an unlimited text messaging plan, intending to keep their current phone number over the next 6 months, and having used text messaging for at least the past 6 months. Recruitment experiences and subsequent steps to refine the Internet-based recruitment strategy are discussed for 4 research activities: online focus groups, content advisory team, beta test, and randomized controlled trial (RCT). Recruitment relied primarily on Facebook advertising. To a lesser extent, Google AdWords and promotion through partner organizations working with AGBM youth were also utilized.ResultsFacebook advertising strategies were regularly adjusted based on preidentified recruitment targets for race, ethnicity, urban-rural residence, and sexual experience. The result was a diverse sample of participants, of whom 30% belonged to a racial minority and 20% were Hispanic. Facebook advertising was the most cost-effective method, and it was also able to reach diverse recruitment goals: recruitment for the first focus group cost an average of US $2.50 per enrolled participant, and it took 9 days to enroll 40 participants; the second focus group cost an average of US $6.96 per enrolled participant, and it took 11 days to enroll 40 participants. Recruitment for the first content advisory team cost an average of US $32.52 per enrolled participant; the second cost US $29.52 per participant. Both recruitment drives required 10 days to enroll 24 participants. For the beta test, recruitment cost an average of US $17.19 per enrolled participant, and it took 16 days to complete enrollment of 20 participants. For the RCT, recruitment cost an average of US $12.54 per enrolled participant, and it took 148 days to enroll 302 participants. Google AdWords campaigns did not result in any enrolled participants of whom the research staff members were aware.ConclusionsInternet-based strategies can be a cost-efficient means to recruit and retain hard-to-reach populations from across the country. With real-time monitoring of participant demographic characteristics, diverse samples can be achieved. Although Facebook advertising was particularly successful in this study, alternative social media strategies can be explored in future research as these media are ever-changing.     

A Mayan founder mutation is a common cause of deafness in Guatemala

Over 5% of the world's population has varying degrees of hearing loss. Mutations in GJB2 are the most common cause of autosomal recessive non‐syndromic hearing loss (ARNHL) in many populations. The frequency and type of mutations are influenced by ethnicity. Guatemala is a multi‐ethnic country with four major populations: Maya, Ladino, Xinca, and Garifuna. To determine the mutation profile of GJB2 in a ARNHL population from Guatemala, we sequenced both exons of GJB2 in 133 unrelated families. A total of six pathogenic variants were detected. The most frequent pathogenic variant is c.131G>A (p.Trp44*) detected in 21 of 266 alleles. We show that c.131G>A is associated with a conserved haplotype in Guatemala suggesting a single founder. The majority of Mayan population lives in the west region of the country from where all c.131G>A carriers originated. Further analysis of genome‐wide variation of individuals carrying the c.131G>A mutation compared with those of Native American, European, and African populations shows a close match with the Mayan population.     

Mesenchymal Stem Cells From Infants Born to Obese Mothers Exhibit Greater Potential for Adipogenesis: The Healthy Start BabyBUMP Project

Maternal obesity increases the risk for pediatric obesity; however, the molecular mechanisms in human infants remain poorly understood. We hypothesized that mesenchymal stem cells (MSCs) from infants born to obese mothers would demonstrate greater potential for adipogenesis and less potential for myogenesis, driven by differences in β-catenin, a regulator of MSC commitment. MSCs were cultured from the umbilical cords of infants born to normal-weight (prepregnancy [pp] BMI 21.1 ± 0.3 kg/m²; n = 15; NW-MSCs) and obese mothers (ppBMI 34.6 ± 1.0 kg/m²; n = 14; Ob-MSCs). Upon differentiation, Ob-MSCs exhibit evidence of greater adipogenesis (+30% Oil Red O stain [ORO], +50% peroxisome proliferator–activated receptor (PPAR)-γ protein; P < 0.05) compared with NW-MSCs. In undifferentiated cells, total β-catenin protein content was 10% lower and phosphorylated Thr41Ser45/total β-catenin was 25% higher (P < 0.05) in Ob-MSCs versus NW-MSCs (P < 0.05). Coupled with 25% lower inhibitory phosphorylation of GSK-3β in Ob-MSCs (P < 0.05), these data suggest greater β-catenin degradation in Ob-MSCs. Lithium chloride inhibition of GSK-3β increased nuclear β-catenin content and normalized nuclear PPAR-γ in Ob-MSCs. Last, ORO in adipogenic differentiating cells was positively correlated with the percent fat mass in infants (r = 0.475; P < 0.05). These results suggest that altered GSK-3β/β-catenin signaling in MSCs of infants exposed to maternal obesity may have important consequences for MSC lineage commitment, fetal fat accrual, and offspring obesity risk.     

Amiodarone in Pediatric Patients

The reported world clinical experience of amiodarone in children is revieived; the known age-dependent electro physiological and pharmacokinetic characteristics of amiodarone are examined; and guidelines for the use of amiodarone in children are suggested.     

A behavioral and 2-deoxyglucose autoradiographic study of the effects of cumulative morphine dose on naloxone precipitated withdrawal in the rat

We have studied regional cerebral metabolism by 2-deoxyglucose autoradiography in 67 brain structures of morphine-dependent rats during fixed dose naloxone precipitated withdrawal. Behavioral indices of withdrawal were studied simultaneously in the same animals used in the cerebral metabolism studies. The effects of cumulative morphine dose (470, 1145 and 2345 mg/kg) with fixed dose (0.5 mg/kg) naloxone precipitated withdrawal upon behavioral and cerebral metabolic measures of the severity of withdrawal were compared.All morphine dependent groups studied exhibited the known behavioral sequelae of naloxone precipitated withdrawal. Qualitative withdrawal signs exhibited by all dependent groups included tachypnea, ptosis, penile erection, ejaculation, diarrhea, urination, salivation, lacrimation, rhinorrhea, and irritability. Quantitative signs of withdrawal for 470, 1145 and 2345 mg/kg cumulative morphine dose groupds were as follows (mean ± S.D.): wet shakes/50 min5.8 ± 1.0; 4.4 ± 0.8; 8.4 ± 1.4; acute weight loss (g)14.0 ± 5.6; 3.4 ± 1.0; 6.8 ± 3.2; ‘jumping’ attempts/50 min10.2 ± 5.7; 25.7 ± 5.9; 3.8 ± 1.2. None of the behavioral measures of morphine withdrawal showed cumulative morphine dose dependency.Metabolic mapping (using 2-deoxyglucose) of functional activity during naloxone precipitated withdrawal revealed several brain regions with cumulative morphine dose dependent increases in glucose utilization. The percentage increase in glucose utilization for several rat brain structures for the 3 cumulative morphine morphine dose treatment groups were as follows: diagonal band 51, 63, 87, medial preoptic area 36, 45, 74; lateral preoptic area 24, 47, 77; globus pallidus 19, 53, 62; paraventricular hypothalamus 56, 98, 118; lateral hypothalamus 65, 84, 112; nucleus accumbens 36, 51, 79; medial septum 49, 50, 88; lateral septum 66, 58, 119; central nucleus amygdala 36, 50, 55; medial mammillary nucleus 25, 87, 103; lateral mammilliary nucleus 27, 82, 97; anteroventral thalamus 63, 87, 107; nucleus centromedianus 34, 68, 78; lateral habenula 93, 119, 158; ventral tegmental area 23, 31, 79; interpeduncular nucleus 59, 94, 121; dorsal raphe 21, 48, 86; median raphe 37, 48, 84. Numerous gray structures additionally analyzed failed to show cumulative morphine dose dependent functional activity changes during fixed dose naloxone precipitated withdrawal. Examples of such unaffected structures, representative of several CNS systems, were the frontal motor and cingulate cortices, anterior hypothalamic area, medial and lateral entorhinal cortices, the dentate gyrus and perforant pathway, medial nucleus of the amygdala, medial geniculate nucleus, red nucleus, the pontine reticular formation, and cranial nerve nuclei III, VII, VIII.Thus, in several brain regions, there were clear cumulative morphine dose dependent increases in glucose utilization. Standard behavioral analyses of withdrawal in the same animals failed to demonstrate clear dose dependency. Metabolic mapping of brain regions showing time and dose effects of opiate drug treatments may facilitate the identification of CNS structures participating in opiate withdrawal phenomena. Once such structures are identified, brain regions of interest can be specifically studied with respect to potential molecular mechanisms of opiate dependence and withdrawal.