Predicting the Onset of Alcohol Use and the Development of Alcohol Use Disorder Among Indigenous Adolescents

Empirical efforts to identify the predictors of drinking behavior among North American Indigenous adolescents are relatively limited. Using longitudinal data, this study considers perceived discrimination, positive drinker prototypes, and peer drinking behavior as risk factors for the onset of alcohol use and development of an alcohol use disorder among 674 Indigenous adolescents as they progressed from early to late adolescence (M age at baseline = 11.11, SD = 0.83). Results showed that positive drinker prototypes and associations with peers who drink increased the risk for the onset of drinking, while perceived discrimination and associations with peers who drink increased the risk for the development of an alcohol use disorder. The theoretical and practical implications of our results are discussed

The Grizzly, September 3, 1984

Japanese Invade UC • Writing for Business: Develop Your Skills • UC Honors Two Faculty Members • Clubs Shine in Activities Fair • The Ultimate Mascot • UC Makes \u2784 Olympics • Presidential Welcome • Calendarhttps://digitalcommons.ursinus.edu/grizzlynews/1119/thumbnail.jp

Geocoding accuracy and the recovery of relationships between environmental exposures and health

<p>Abstract</p> <p>Background</p> <p>This research develops methods for determining the effect of geocoding quality on relationships between environmental exposures and health. The likelihood of detecting an existing relationship – statistical power – between measures of environmental exposures and health depends not only on the strength of the relationship but also on the level of positional accuracy and completeness of the geocodes from which the measures of environmental exposure are made. This paper summarizes the results of simulation studies conducted to examine the impact of inaccuracies of geocoded addresses generated by three types of geocoding processes: a) addresses located on orthophoto maps, b) addresses matched to TIGER files (U.S Census or their derivative street files); and, c) addresses from E-911 geocodes (developed by local authorities for emergency dispatch purposes).</p> <p>Results</p> <p>The simulated odds of disease using exposures modelled from the highest quality geocodes could be sufficiently recovered using other, more commonly used, geocoding processes such as TIGER and E-911; however, the strength of the odds relationship between disease exposures modelled at geocodes generally declined with decreasing geocoding accuracy.</p> <p>Conclusion</p> <p>Although these specific results cannot be generalized to new situations, the methods used to determine the sensitivity of results can be used in new situations. Estimated measures of positional accuracy must be used in the interpretation of results of analyses that investigate relationships between health outcomes and exposures measured at residential locations. Analyses similar to those employed in this paper can be used to validate interpretation of results from empirical analyses that use geocoded locations with estimated measures of positional accuracy.</p

Leveraging Online Learning Resources to Teach Core Research Skills to Undergraduates at a Diverse Research University

Int J Exerc Sci 3(2) : 49-54, 2010. Today’s students have unique learning needs and lack knowledge of core research skills. In this program report, we describe an online approach that we developed to teach core research skills to freshman and sophomore undergraduates. Specifically, we used two undergraduate kinesiology (KIN) courses designed to target students throughout campus (KIN1304: Public Health Issues in Physical Activity and Obesity) and specifically kinesiology majors (KIN1252: Foundations of Kinesiology). Our program was developed and validated at the 2nd largest ethnically diverse research university in the United States, thus we believe that it would be effective in a variety of student populations

Longitudinal, Diet-induced Weight Gain is Associated with Increased Blood Monocytes and Reduced TLR4 Expression

Excessive weight gain increases systemic inflammation resulting in increased disease risk. Toll-like receptor 4 (TLR4) reportedly mediates increases in inflammation; however, its role has not been fully evaluated. Objective. The purpose of this study was to determine the longitudinal effect of diet-induced weight gain on blood monocyte concentration and cell-surface TLR4 expression. Research Methods & Procedures. Male CD-1 mice were randomly assigned to high-fat (HF, n = 12) or low-fat (LF, n = 13) groups. Non-lethal, saphenous vein blood samples were collected at 0, 4, 8 and 12 weeks of treatment. Three-color flow cytometry was used to measure monocyte (CD11b+/CD14+) concentration and TLR4 cells-surface expression. Data were analyzed with a repeated measures ANOVA; significance was set at P\u3c0.05. Results. Body weight at week 12 was 21% greater in HF than LF (P\u3c0.05). At week 12 HF had 155% more monocytes (P\u3c0.05) with 24% less TLR4; Monocyte concentration and body weight at week 12 was negatively correlated with TLR4 gMFI (P\u3c0.05). Conclusions. The observed effects of high-fat feeding on blood monocytes are consistent with a phenotype, which may be associated with premature morbidity. The observed monocyte responses may be associated with immune dysfunction and diminished response to infection

Aerobic Exercise Training May Not Offset the Pro-inflammatory Effects of a High Fat Feeding

Aerobic Exercise Training May Not Offset the Pro-inflammatory Effects of a High Fat Feeding. Katie C. Carpenter, Lisa Esposito, Kelley A. Strohacker, Richard J. Simpson, Brian K. McFarlin. University of Houston, Houston, TX Increased adiposity is associated with an increase in systemic inflammation, which is involved in the pathophysiology of various disease states. A current hypothesis in our laboratory suggests that the toll-like receptor 4 (TLR4) pathway may link physical activity and systemic inflammation. PURPOSE: The primary purpose was to determine if 6-weeks of aerobic exercise training (5 days per week, 1 hour per day. 21-22m/min) would limit the increase in systemic inflammation resulting from high-fat (60% of calories from fat) feeding. A secondary purpose was to determine if changes in cell-surface TLR4 expression would account for observed differences in inflammatory status between mice which exercise and those that remain sedentary. METHODS: 36 CD-1 male mice were randomly assigned to one of three groups (N=12/group): HF (remained sedentary and consumed a high-fat chow (60% fat)), HF-EX (consumed the high-fat chow and underwent an aerobic exercise intervention (running 4.56±0.08 h/week for 6 weeks, or LF (sedentary and consumed a low-fat chow (10% fat)). Key outcome measurements were made on weekly saphenous vein blood samples (~40 uL) using 3-color flow cytometry. Blood glucose and cholesterol concentration were analyzed by an enzymatic assay. RESULTS: Absolute and percent body weight gain over 6-weeks was similar between HF and HF-EX, but significantly greater than LF (P\u3c0.001). HF and HF-EX had 66% more leukocytes than LF at weeks 3-5 (P\u3c0.0001). HF and HF-EX had 145% greater CD11b+/14+/TLR4+ cells than LF (P=0.001). There was no difference in the concentration of CD11b+ cells expressing IL-6 or TNF-alpha following LPS-stimulation between HF and HF-EX. No significant difference was found for blood glucose and cholesterol concentrations between groups. CONCLUSIONS: Exercise training did not prevent weight gain during 6-weeks of high fat feeding. Since HF and HF+EX gained a similar amount of weight, they did not differ with regarding to blood monocytes expressing TLR4. Both HF and HF+EX were elevated above LF. More research is needed to determine how changes in the blood relate to changes in peripheral tissue compartments

Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors

AbstractPurpose: Pathologic remodeling of the extracellular matrix is a critical mechanism in the development and progression of abdominal aortic aneurysms (AAAs). Although angiotensin-converting enzyme (ACE) inhibitors are known to alter vascular wall remodeling in other conditions, their effects on AAAs are unknown. In this study we assessed the effect of ACE inhibitors in a rodent model of aneurysm development. Methods: Male Wistar rats underwent transient aortic perfusion with porcine pancreatic elastase, followed by treatment with one of three ACE inhibitors (captopril [CP], lisinopril [LP], or enalapril [EP]), an angiotensin (AT)1 receptor antagonist (losartan [LOS]), or water alone (9 rats in each group). Blood pressure and aortic diameter (AD) were measured before elastase perfusion and on day 14, with an AAA defined as an increase in AD (ΔAD) of more than 100%. The structural features of the aortic wall were examined by means of light microscopy. Results: Aneurysmal dilatation consistently developed within 14 days of elastase perfusion in untreated rats, coinciding with the development of a transmural inflammatory response and destruction of the elastic media (mean ΔAD, 223% ± 28%). All three ACE inhibitors prevented AAA development (mean ΔAD: CP, 67% ± 4%; LP, 18% ± 12%; and EP, 14% ± 3%; each P <.05 vs controls). ACE inhibitors also attenuated the degradation of medial elastin without diminishing the inflammatory response. Surprisingly, the aneurysm-suppressing effects of ACE inhibitors were dissociated from their effects on systemic hemodynamics, and LOS had no significant effect on aneurysm development compared with untreated controls (mean ΔAD, 186% ± 19%). Conclusion: Treatment with ACE inhibitors suppresses the development of elastase-induced AAAs in the rat. Although this is associated with the preservation of medial elastin, the mechanisms underlying these effects appear to be distinct from hemodynamic alterations alone or events mediated solely by AT1 receptors. Further studies are needed to elucidate how ACE inhibitors influence aortic wall matrix remodeling during aneurysmal degeneration. (J Vasc Surg 2001;33:1057-64.

Can translocated native fishes retain their trophic niche when confronted with a resident invasive?

Diet interactions between native and non-native fishes may influence the establishment of native species within their historical range (i.e., reintroduction). Therefore, we illustrated the food web structure of and followed the transition of the federally endangered humpback chub Gila cypha into a novel food web following translocation and determined the potential for a non-native species, rainbow trout Oncorhynchus mykiss, to influence translocation success. Humpback chub and rainbow trout used resources high in the food web and assimilated similar proportions of native fishes, suggesting non-native rainbow trout may occupy an ecological role similar to humpback chub. Subsequently, humpback chub may be well suited to colonise tributaries because of their ability to consume resources high in the food web. Additionally, diet partitioning may occur between all members of the fish community as indicated by separation in trophic niche space and little trophic overlap; although all species, particularly bluehead sucker Catostomus discobolus, used a broad range of food resources. Rainbow trout stomach content analysis corroborated stable isotope analysis and suggested rainbow trout diet consisted of aquatic and terrestrial macroinvertebrates, while larger rainbow trout (\u3e120 mm total length) consumed a greater proportion of fish (incidence of piscivory = 5.3%). Trophic interactions may reveal an underutilized niche space or biotic resistance to the establishment of translocated native fishes. Continued translocation of humpback chub into tributaries appears to be one option for conservation. However, successful establishment of humpback chub may depend on continued removal of non-native trout, increasing availability of diet sources at higher trophic levels

Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors

AbstractPurpose: Pathologic remodeling of the extracellular matrix is a critical mechanism in the development and progression of abdominal aortic aneurysms (AAAs). Although angiotensin-converting enzyme (ACE) inhibitors are known to alter vascular wall remodeling in other conditions, their effects on AAAs are unknown. In this study we assessed the effect of ACE inhibitors in a rodent model of aneurysm development. Methods: Male Wistar rats underwent transient aortic perfusion with porcine pancreatic elastase, followed by treatment with one of three ACE inhibitors (captopril [CP], lisinopril [LP], or enalapril [EP]), an angiotensin (AT)1 receptor antagonist (losartan [LOS]), or water alone (9 rats in each group). Blood pressure and aortic diameter (AD) were measured before elastase perfusion and on day 14, with an AAA defined as an increase in AD (ΔAD) of more than 100%. The structural features of the aortic wall were examined by means of light microscopy. Results: Aneurysmal dilatation consistently developed within 14 days of elastase perfusion in untreated rats, coinciding with the development of a transmural inflammatory response and destruction of the elastic media (mean ΔAD, 223% ± 28%). All three ACE inhibitors prevented AAA development (mean ΔAD: CP, 67% ± 4%; LP, 18% ± 12%; and EP, 14% ± 3%; each P <.05 vs controls). ACE inhibitors also attenuated the degradation of medial elastin without diminishing the inflammatory response. Surprisingly, the aneurysm-suppressing effects of ACE inhibitors were dissociated from their effects on systemic hemodynamics, and LOS had no significant effect on aneurysm development compared with untreated controls (mean ΔAD, 186% ± 19%). Conclusion: Treatment with ACE inhibitors suppresses the development of elastase-induced AAAs in the rat. Although this is associated with the preservation of medial elastin, the mechanisms underlying these effects appear to be distinct from hemodynamic alterations alone or events mediated solely by AT1 receptors. Further studies are needed to elucidate how ACE inhibitors influence aortic wall matrix remodeling during aneurysmal degeneration. (J Vasc Surg 2001;33:1057-64.

A Longitudinal Examination of the Measurement Properties and Predictive Utility of the Center for Epidemiologic Studies Depression Scale Among North American Indigenous Adolescents

We examined the longitudinal measurement properties and predictive utility of the Center for Epidemiologic Studies Depression Scale (CES-D) from early to late adolescence among a sample of North American Indigenous youths. Participants were 632 North American Indigenous adolescents (n = 632; 50.3% girls; M age at baseline = 11.11 years) participating in an 8-year, 8-wave longitudinal study. Via in-person interviews, participants completed the CES-D at Waves 1, 3, 5, and 7, and the major depressive disorder (MDD) module of the Diagnostic Interview Schedule for Children at Waves 1, 4, 6, and 8. Confirmatory factor analyses indicated that responses to the CES-D were similarly explained by 2-, 3-, and 4-factor models, as well as a 1-factor model with correlations between the error variances for the positively worded items. Longitudinal measurement equivalence analyses indicated full structural (i.e., factor structure), metric (i.e., factor loadings), and scalar (i.e., observed item intercepts) equivalence for each factor structure. Substantive analyses showed that the CES-D was significantly associated with MDD both concurrently and prospectively, although these effects were smaller than might be expected. Finally, the CES-D negative affect and somatic complaints subscales were the strongest and most consistent predictors of MDD. Among our sample of North American Indigenous youths, the measurement properties of the CES-D were stable from early to late adolescence. Moreover, somatic difficulties and depressed affect were the strongest predictors of MDD