Informing women about the risks of exposing babies to tobacco smoke: outreach and education efforts using Facebook "boost posts".

Maternal smoking is associated with a host of negative health outcomes, including an increased risk of children developing attention-deficit/hyperactivity disorder (ADHD). This study evaluated the efficacy of health messages disseminated through Facebook Ads focused on reducing tobacco smoke exposure during pregnancy. Two message versions were promoted via post advertisements on Facebook-a static infographic and a video containing an animated version of the infographic. The reach of and engagement with each message version was evaluated. Comments made to the posts were assessed using content analysis. The infographic reached approximately 60,000 people and the video reached about 16,000 people. The average costs were $10.00 and $40.00 per 1,000 people reached for the infographic- and video-based posts, respectively. While there was no engagement with the video, the infographic was liked (n = 157), given alternative likes (n = 59), shared (n = 171 to 341), and commented on (n = 221). About one-quarter of comments contained a personal narrative and mentions of health history related to ADHD and/or smoking. Comments were more often negative (than positive) (16.6% vs 3.9%) and expressed skepticism more often than message acceptance (21.5% vs 12.2%). Facebook users were more responsive to the infographic (compared to the video) and static posts were a preferred channel (i.e., higher engagement at a lower cost) to disseminate messages when using the boost post feature on Facebook for health education. Our review of the comments provided insights into message acceptance and guidance for future social media-based health message campaigns. However, it is not known whether and if so, how, these findings on message exposure would correlate with behavioral intentions or changes in behavior, such as intentions to quit smoking or smoking cessation.

Development of an Online Experiment Platform for High School Biology.

We developed a novel online platform, Rex (Real experiments) that immerses students in a scientific investigative process. Rex is a virtual web-based biological science experiment platform, hosted by real scientists, and uses actual lab experiments that generate real data for students to collect, analyze, and interpret. Seven neuroscience experiments use zebrafish and rats as model systems to study the effects of drugs such as tetrahydrocannabinol (THC), caffeine, alcohol, and cigarette smoke, which are of interest to high school students. We carried out a small field-test of Rex in a variety of high school biology classrooms (e.g., standard, honors, AP, anatomy/physiology) to obtain student and teacher feedback about the implementation and usability of the program. We also assessed student situational interest (SI) to determine whether the Rex experiment captured students' attention, and whether it was an enjoyable and meaningful experience. Overall, students reported a moderate level of SI after participating in the Rex experiments. Situational interest did not differ across teachers, class section, class level, or the type of experiment. In addition, we present details of the technical issues encountered in the classroom, and we provide guidance to readers who may want to use the resource in their classrooms.

Science expectancy, value, and cost profiles and their proximal and distal relations to undergraduate science, technology, engineering, and math persistence.

Despite efforts to attract and maintain diverse students in the science, technology, engineering and math (STEM) pipeline, issues with attrition from undergraduate STEM majors persist. The aim of this study was to examine how undergraduate science students' competence beliefs, task values, and perceived costs in science combine into motivational profiles and to consider how such profiles relate to short and long-term persistence outcomes in STEM. We also examined the relations between underrepresented group membership and profile membership. Using latent profile analysis, we identified three profiles that characterized 600 participants' motivation during their first semester in college: Moderate All, Very High Competence/Values-Low Effort Cost, and High Competence/Values-Moderate Low Costs. The Moderate All profile was associated with the completion of fewer STEM courses and lower STEM GPAs relative to the other profiles after one year and after four years of college. Furthermore, underrepresented minority students were overrepresented in the Moderate All profile. Findings contribute to our understanding of how science competence beliefs, task values, and perceived costs may coexist and what combinations of these variables may be adaptive or deleterious for STEM persistence and achievement.

Alcohol Pharmacology Education Partnership: Using Chemistry and Biology Concepts To Educate High School Students about Alcohol.

We developed the Alcohol Pharmacology Education Partnership (APEP), a set of modules designed to integrate a topic of interest (alcohol) with concepts in chemistry and biology for high school students. Chemistry and biology teachers (n = 156) were recruited nationally to field-test APEP in a controlled study. Teachers obtained professional development either at a conference-based workshop (NSTA or NCSTA) or via distance learning to learn how to incorporate the APEP modules into their teaching. They field-tested the modules in their classes during the following year. Teacher knowledge of chemistry and biology concepts increased significantly following professional development, and was maintained for at least a year. Their students (n = 14 014) demonstrated significantly higher scores when assessed for knowledge of both basic and advanced chemistry and biology concepts compared to students not using APEP modules in their classes the previous year. Higher scores were achieved as the number of modules used increased. These findings are consistent with our previous studies, demonstrating higher scores in chemistry and biology after students use modules that integrate topics interesting to them, such as drugs (the Pharmacology Education Partnership).

Relationships among factual and perceived knowledge of harms of waterpipe tobacco, perceived risk, and desire to quit among college users.

Waterpipe tobacco smoking is increasing in the United States among college students. Through a web-based survey, we explored associations among factual and perceived knowledge, perceived risks and worry about harm and addiction, and desire to quit among 316 college waterpipe tobacco smoking users. Overall, factual knowledge of the harm of waterpipe tobacco smoking was poor, factual and perceived knowledge was weakly correlated, both forms of knowledge were related inconsistently to perceived risks and worry, and neither form of knowledge was associated with the desire to quit. Findings provide preliminary insights as to why knowledge gaps may not predict cessation among waterpipe users.

Affecting perceptions of harm and addiction among college waterpipe tobacco smokers.

INTRODUCTION: The spread of waterpipe tobacco use among youth may be due in part to perceptions that waterpipe tobacco use is safer than other tobacco products, such as cigarettes. In two pilot studies, we sought to modify college waterpipe smokers' perceived risks and worry about waterpipe tobacco smoking. METHODS: We conducted two web-based studies that varied whether college waterpipe users received information on (a) spread of and use of flavored tobacco in waterpipe and (b) harms of waterpipe smoking. Study 1 (N = 91) tested the "incremental" effects on perceptions of risk and worry of adding information about harms of waterpipe smoking to information on the spread of waterpipe and use of flavorings in the tobacco. Study 2 (N = 112) tested the effects on perceptions of risk and worry of reviewing information about harms of waterpipe smoking compared to a no information control group. In Study 1 only, we assessed as part of a 6-month follow-up (n = 70) the percentage of participants who reported no longer using waterpipe. RESULTS: Pooling data from both studies, participants who received information about the harms of waterpipe smoking reported greater perceived risk and worry about harm and addiction and expressed a stronger desire to quit. In Study 1, 62% of participants in the experimental group versus 33% in the control group reported having stopped waterpipe use. CONCLUSIONS: These are the first studies to show that perceptions of addiction and harm from waterpipe use can be modified using minimally intensive interventions; such interventions show promise at decreasing waterpipe use.

Teaching High School Chemistry in the Context of Pharmacology Helps Both Teachers and Students Learn.

Few studies demonstrate the impact of teaching chemistry embedded in a context that has relevance to high school students. We build upon our prior work showing that pharmacology topics (i.e., drugs), which are inherently interesting to high school students, provide a useful context for teaching chemistry and biology. In those studies, teachers were provided professional development for the Pharmacology Education Partnership (PEP) in an onsite venue (either five-day or one-day workshop). Given financial difficulties to travel, teachers have asked for alternatives for professional development. Thus, we developed the same PEP training workshop using a distance learning (DL) (two-way live video) approach. In this way, 121 chemistry and biology teachers participated in the DL workshops to learn how to incorporate the PEP modules into their teaching. They field-tested the modules over the year in high school chemistry and biology classes. Teacher knowledge of chemistry and biology increased significantly after the workshop and was maintained for at least a year. Their students (N = 2309) demonstrated a significant increase in knowledge of chemistry and biology concepts, with higher scores as the number of modules used increased. The increase in both teacher and student knowledge in these subjects was similar to that found previously when teachers were provided with onsite professional development.

Direction discovery: A science enrichment program for high school students.

Launch into education about pharmacology (LEAP) is an inquiry-based science enrichment program designed to enhance competence in biology and chemistry and foster interest in science careers especially among under-represented minorities. The study of how drugs work, how they enter cells, alter body chemistry, and exit the body engages students to conceptualize fundamental precepts in biology, chemistry, and math. Students complete an intensive three-week course in the fundamentals of pharmacology during the summer followed by a mentored research component during the school year. Following a 5E learning paradigm, the summer course captures student interest by introducing controversial topics in pharmacology and provides a framework that guides them to explore topics in greater detail. The 5E learning cycle is recapitulated as students extend their knowledge to design and to test an original research question in pharmacology. LEAP students demonstrated significant gains in biology and chemistry knowledge and interests in pursuing science. Several students earned honors for the presentation of their research in regional and state science fairs. Success of the LEAP model in its initial 2 years argues that coupling college-level coursework of interest to teens with an authentic research experience enhances high school student success in and enthusiasm for science.

Impaired firing and sodium channel function in CA1 hippocampal interneurons after transient cerebral ischemia.

Although interneurons in area CA1 of the hippocampus are less vulnerable to cerebral ischemia than CA1 pyramidal cells, it is not clear whether their relatively intact cellular morphology implies preservation of normal function. As maintenance of cellular excitability and firing properties is essential for interneurons to regulate neural networks, we investigated these aspects of interneuronal function after transient cerebral ischemia in rats. Cerebral ischemia in rats was induced for 8 mins by a combination of bilateral common carotid artery occlusion and hypovolemic hypotension, and whole cell patch clamp recordings were made in hippocampal slices prepared 24 h after reperfusion. Interneurons located within stratum pyramidale of area CA1 exhibited normal membrane properties and action potentials under these conditions. However, their excitability had declined, as evidenced by an increased action potential threshold and a rightward shift in the relationship between injected depolarizing current and firing rate. Voltage-clamp experiments revealed that transient cerebral ischemia reduced the peak Na(+) current and shifted Na(+) channel activation to more depolarized values, but did not alter steady-state inactivation of the channel. Double immunofluorescence cytochemistry showed that transient cerebral ischemia also reduced Na(v)1.1 subunit immunoreactivity in interneurons that coexpressed parvalbumin. We conclude that transient cerebral ischemia renders CA1 interneurons less excitable, that depressed excitability involves impaired Na(+) channel activation and that Na(+) channel dysfunction is explained, at least in part, by reduced expression of the Na(v)1.1 subunit. These changes may promote interneuron survival, but might also contribute to pyramidal cell death.

The chloride transporter Na(+)-K(+)-Cl- cotransporter isoform-1 contributes to intracellular chloride increases after in vitro ischemia.

Ischemic episodes in the CNS cause significant disturbances in neuronal ionic homeostasis. To directly measure changes in intracellular Cl- concentration ([Cl-]i) during and after ischemia, we used Clomeleon, a novel ratiometric optical indicator for Cl-. Hippocampal slices from adult transgenic mice expressing Clomeleon in hippocampal neurons were subjected to 8 min of oxygen-glucose deprivation (OGD) (an in vitro model for ischemia) and reoxygenated in the presence of glucose. This produced mild neuronal damage 3 h later that was prevented when the extracellular [Cl-] was maintained at 10 mm during reoxygenation. OGD induced a transient decrease in fluorescence resonance energy transfer within Clomeleon, indicating an increase in [Cl-]i. During reoxygenation, there was a partial recovery in [Cl-]i, but [Cl-]i rose again 45 min later. To investigate sources of Cl- accumulation, we examined the effects of Cl- transport inhibitors on the rises in [Cl-]i during and after OGD. Bumetanide and furosemide, which inhibit Cl- influx through the Na(+)-K(+)-Cl- cotransporter isoform-1 (NKCC-1) and efflux through the K(+)-Cl- cotransporter isoform-2, were unable to inhibit the first rise in [Cl-]i, yet entirely prevented the secondary rise in [Cl-]i during reoxygenation. In contrast, picrotoxin, which blocks the GABA-gated Cl- channel, did not inhibit the secondary rise in [Cl-]i after OGD. [Cl-]i increases during reoxygenation were accompanied by an increase in phosphorylation of NKCC-1, an indication of increased NKCC-1 activity after OGD. We conclude that NKCC-1 plays an important role in OGD-induced Cl- accumulation and subsequent neuronal damage.

Depressed responses to applied and synaptically-released GABA in CA1 pyramidal cells, but not in CA1 interneurons, after transient forebrain ischemia.

Transient cerebral ischemia kills CA1 pyramidal cells of the hippocampus, whereas most CA1 interneurons survive. It has been proposed that calcium-binding proteins, neurotrophins, and/or inhibitory neuropeptides protect interneurons from ischemia. However, different synaptic responses early after reperfusion could also underlie the relative vulnerabilities to ischemia of pyramidal cells and interneurons. In this study, we used gramicidin perforated patch recording in ex vivo slices to investigate gamma-aminobutyric acid (GABA) synaptic function in CA1 pyramidal cells and interneurons 4 h after a bilateral carotid occlusion accompanied by hypovolemic hypotension. At this survival time, the amplitudes of both miniature inhibitory postsynaptic currents (mIPSCs) and GABA-evoked currents were reduced in CA1 pyramidal cells, but not in CA1 interneurons. In addition, the mean rise time of mIPSCs was reduced in pyramidal cells. The reversal potential for the GABA current (E(GABA)) did not shift toward depolarizing values in either cell type, indicating that the driving force for chloride was unchanged at this survival time. We conclude that early during reperfusion GABAergic neurotransmission is attenuated exclusively in pyramidal neurons. This is likely explained by reduced GABAA receptor sensitivity or clustering and possibly also reduced GABA release, rather than by an elevation of intracellular chloride. Impaired GABA function may contribute to ischemic neuronal death by enhancing the excitability of CA1 pyramidal cells and facilitating N-methyl-D-aspartic acid channel opening. Therefore, normalizing GABAergic function might be a useful pharmacological approach to counter excessive, and potentially excitotoxic, glutamatergic activity during the postischemic period.

A randomized trial comparing the effects of self-help materials and proactive telephone counseling on teen smoking cessation.

We conducted a 2-arm randomized trial to test the efficacy of self-help materials with or without proactive telephone counseling to increase cessation among teen smokers. Teen smokers (N = 402) recruited from 11 shopping malls and 1 amusement park in the southeastern United States were randomized to 1 of 2 groups: written self-help material plus video; or written self-help material, video, and telephone counseling. Cessation rates based on 7-day point-prevalent abstinence for the self-help and counseling arms were 11% and 16%, respectively (p = .25), at 4 months postbaseline and 19% and 21%, respectively (p = .80), at 8 months postbaseline. Sustained abstinence, reflecting 7-day abstinence at both time points, in the self-help and counseling arms was 7% and 9% (p = .59). Results suggest that minimal self-help cessation approaches that target youth have comparable success to that shown among adult smokers. However, refinements in telephone-counseling approaches may be needed to achieve the success observed in adult populations.

Chloride transport inhibitors influence recovery from oxygen-glucose deprivation-induced cellular injury in adult hippocampus.

Cerebral ischemia in vivo or oxygen-glucose deprivation (OGD) in vitro are characterized by major disturbances in neuronal ionic homeostasis, including significant rises in intracellular Na(+), Ca(2+), and Cl(-) and extracellular K(+). Recently, considerable attention has been focused on the cation-chloride cotransporters Na-K-Cl cotransporter isoform I (NKCC-1) and K-Cl cotransporter isoform II (KCC2), as they may play an important role in the disruption of ion gradients and subsequent ischemic damage. In this study, we examined the ability of cation-chloride transport inhibitors to influence the biochemical (i.e. ATP) and histological recovery of neurons in adult hippocampal slices exposed to OGD. In the hippocampus, 7 min of OGD caused a loss of ATP that recovered partially (approximately 50%) during 3 h of reoxygenation. Furosemide, which inhibits the NKCC-1 and KCC2 cotransporters, and bumetanide, a more specific NKCC-1 inhibitor, enhanced ATP recovery when measured 3 h after OGD. Furosemide and bumetanide also attenuated area CA1 neuronal injury after OGD. However, higher concentrations of these compounds appear to have additional non-specific toxic effects, limiting ATP recovery following OGD and promoting neuronal injury. The KCC2 cotransporter inhibitor DIOA and the Cl(-) ATPase inhibitor ethacrynic acid caused neuronal death even in the absence of OGD and promoted cytochrome c release from isolated mitochondria, indicating non-specific toxicities of these compounds.

Changes in intracellular chloride after oxygen-glucose deprivation of the adult hippocampal slice: effect of diazepam.

Ischemic injury to the CNS results in loss of ionic homeostasis and the development of neuronal death. An increase in intracellular Ca2+ is well established, but there are few studies of changes in intracellular Cl- ([Cl-]i) after ischemia. We used an in vitro model of cerebral ischemia (oxygen-glucose deprivation) to examine changes in [Cl-]i and GABA(A) receptor-mediated responses in hippocampal slices from adult rats. Changes in [Cl-]i were measured in area CA1 pyramidal neurons using optical imaging of 6-methoxy-N-ethylquinolinium chloride, a Cl--sensitive fluorescent indicator. Oxygen-glucose deprivation induced an immediate rise in [Cl-]i, which recovered within 20 min. A second and more prolonged rise in [Cl-]i occurred within the next hour, during which postsynaptic field potentials failed to recover. The sustained increase in [Cl-]i was not blocked by GABA(A) receptor antagonists. However, oxygen-glucose deprivation caused a progressive downregulation of the K+-Cl- cotransporter (KCC2), which may have contributed to the Cl- accumulation. The rise in [Cl-]i was accompanied by an inability of the GABA(A) agonist muscimol to cause Cl- influx. In vivo, diazepam is neuroprotective when given early after ischemia, although the mechanism by which this occurs is not well understood. Here, we added diazepam early after oxygen-glucose deprivation and prevented the downregulation of KCC2 and the accumulation of [Cl-]i. Consequently, both GABA(A) responses and synaptic transmission within the hippocampus were restored. Thus, after oxygen-glucose deprivation, diazepam may decrease neuronal excitability, thereby reducing the energy demands of the neuron. This may prevent the activation of downstream cell death mechanisms and restore Cl- homeostasis and neuronal function

Modulation of the GABA(A)-gated chloride channel by reactive oxygen species.

The accumulation of reactive oxygen species during cellular injury leads to oxidative stress. This can have profound effects on ionic homeostasis and neuronal transmission. Gamma-aminobutyric acid (GABA) neurotransmission is sensitive to reactive oxygen species, but most studies have indicated that this is due to alterations in GABA release. Here, we determined whether reactive oxygen species can alter GABA(A) receptor-gated Cl- channels in the adult hippocampus. First, we measured the effects of hydrogen peroxide on intracellular Cl- using UV laser scanning confocal microscopy and the Cl(-)-sensitive probe, 6-methoxy-N-ethylquinolium iodide (MEQ). Superfusion of adult rat hippocampal slices with hydrogen peroxide for 10 min decreased MEQ fluorescence (elevation in [Cl-]i) significantly in area CA1 pyramidal cell soma. Alterations in [Cl-]i were prevented by the vitamin E analog Trolox, an antioxidant that scavenges free radicals. After exposure of slices to hydrogen peroxide, the ability of the GABA agonist muscimol to increase [Cl-]i was attenuated. To determine if GABA(A) receptors were sensitive to oxidative insults, the effect of hydrogen peroxide on the binding of [35S]t-butylbicyclophosphorothionate (TBPS) to GABA-gated Cl- channels was measured using receptor autoradiography and homogenate binding assays. Hydrogen peroxide inhibited [35S]TBPS binding in a regionally selective manner, with the greatest inhibition in cerebral cortex, hippocampus and striatum, areas vulnerable to oxidative stress. Similarly, xanthine and xanthine oxidase, which generate superoxide radicals, reduced [35S]TBPS binding in these regions. The effect of hydrogen peroxide on [35S]TBPS binding was non-competitive and was prevented by Trolox and the iron chelator, deferoxamine. We conclude that reactive oxygen species may compromise GABA(A)-mediated neuronal inhibition via interaction with pre and postsynaptic sites. A reduction in GABA(A)-gated Cl- channel function during periods of oxidative stress may contribute to the development of neuronal damage.