Exploring mediation pathways on the relationship between acculturation and binge eating among Latino adolescents.

The objective of this study was to explore the mediating effects of emotional eating, restrained eating, and external eating on the relationship between acculturation and binge eating among Latino adolescents. Adolescents who self-identified as Latino (N = 285) at public high schools in Southern California were recruited and completed a self-report survey. Acculturation was assessed using the 8-item Acculturation, Habits, Interests for Multicultural Adolescents (AHIMSA) scale for adolescents, mediators were assessed using Dutch Eating Behavior Questionnaire (DEBQ), and binge eating was assessed using a 13-item Eating Disorder Diagnostic Scale. A bootstrapped multiple mediation model was used to test mediation pathways. Findings suggest that individually each eating style-emotional, restrained and external eating pathway did not reach significance singly, but that jointly, their combined effect was significant with a total indirect effect (B = 0.15, CI 0.01-0.30) indicating an additive effect of the three eating styles. Future research should examine additional mediators of the relationship between acculturation and binge eating.

Threshold score for the self-report Pediatric Distress Thermometer Rating Scale in childhood cancer patients.

OBJECTIVE: Although there is enthusiasm for identifying and treating psychosocial problems in childhood cancer patients, there are few validated instruments to help providers identify at-risk children for further assessment. The study objective was to evaluate the sensitivity and specificity of the self-report pediatric Distress Thermometer Rating Scale (Peds DTRS) in childhood cancer survivors and identify a threshold score to help providers classify pediatric patients. METHODS: We evaluated 54 children 7-17 years old using 178 Peds DTRS longitudinal data points from the cohort that was used for the original pediatric adaptation of the DTRS. We compared Peds DTRS scores against two established standardized measures using a generalized linear mixed model to deal with the dependency in the longitudinal data to estimate ROC curves and related statistics. RESULTS: Results indicate that a score of 3 is a reasonable cutoff to identify distress with children 7-17 years old. This cutoff yielded high sensitivity (87.0%) and specificity (79.7%) using the PedsQL Emotional Domain score as the standard. Similar results were obtained using the CDI as the standard, but we are cautious as very few CDI scores reached the cutoff criterion. Exploratory analysis highlighted clinical factors that correlate with increased distress measured using the Peds DTRS. CONCLUSIONS: The Peds DTRS is a very brief, convenient, and rapid screening tool for global distress in children. Further investigation of the Peds DTRS and other tools can improve the ability of providers to prevent and treat the negative emotional consequences of cancer and improve the quality of survivorship.

Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction.

Myocardial infarction (MI), a leading cause of death around the world, displays a complex pattern of inheritance. When MI occurs early in life, genetic inheritance is a major component to risk. Previously, rare mutations in low-density lipoprotein (LDL) genes have been shown to contribute to MI risk in individual families, whereas common variants at more than 45 loci have been associated with MI risk in the population. Here we evaluate how rare mutations contribute to early-onset MI risk in the population. We sequenced the protein-coding regions of 9,793 genomes from patients with MI at an early age (≤50 years in males and ≤60 years in females) along with MI-free controls. We identified two genes in which rare coding-sequence mutations were more frequent in MI cases versus controls at exome-wide significance. At low-density lipoprotein receptor (LDLR), carriers of rare non-synonymous mutations were at 4.2-fold increased risk for MI; carriers of null alleles at LDLR were at even higher risk (13-fold difference). Approximately 2% of early MI cases harbour a rare, damaging mutation in LDLR; this estimate is similar to one made more than 40 years ago using an analysis of total cholesterol. Among controls, about 1 in 217 carried an LDLR coding-sequence mutation and had plasma LDL cholesterol > 190 mg dl(-1). At apolipoprotein A-V (APOA5), carriers of rare non-synonymous mutations were at 2.2-fold increased risk for MI. When compared with non-carriers, LDLR mutation carriers had higher plasma LDL cholesterol, whereas APOA5 mutation carriers had higher plasma triglycerides. Recent evidence has connected MI risk with coding-sequence mutations at two genes functionally related to APOA5, namely lipoprotein lipase and apolipoprotein C-III (refs 18, 19). Combined, these observations suggest that, as well as LDL cholesterol, disordered metabolism of triglyceride-rich lipoproteins contributes to MI risk.

Social-ecological predictors of school functioning in Hispanic children treated for cancer with central nervous system-directed therapies.

BACKGROUND: Children with brain tumor or acute leukemia are at risk for neurotoxic side effects associated with their cancer therapies. These long-term deficits include poor health-related quality of life (HRQOL) in school and lower educational achievement. Although social-ecological factors may impact these outcomes, it is not known which factors play a role. Our objective was to evaluate the factors affecting school HRQOL in Hispanic childhood cancer survivors, an important at-risk group. PROCEDURE: Multivariable regression analyses examined whether selected social-ecological factors contribute toward suboptimal school HRQOL in 73 Hispanic children treated with central nervous system (CNS)-directed cancer therapies after accounting for effects associated with established cancer-related risk factors. RESULTS: Consistent with expectations from prior research, in our multivariate analysis, the cancer-related factors of having a brain tumor diagnosis and being younger at cancer diagnosis were significant predictors of reduced parent-reported school HRQOL (F(2,65) = 5.46, P < .01) and accounted for 14% of the variance. Adding the social-ecological variables of parent education, child motivation, and parental knowledge accounted for an additional 25% of the variance in school HRQOL, where higher levels were associated with better child school HRQOL. Parenting knowledge was a contributor even after controlling for effects associated with the other variables in the model (F(1,62) = 4.88, P < .05). CONCLUSIONS: Cancer survivorship care should incorporate parent education interventions to enhance the child's school functioning, particularly for Hispanic childhood cancer survivors from predominantly Spanish-speaking families. Future research should consider other at-risk groups and incorporate social-ecological indicators to predict HRQOL outcomes.

An Examination of Family Variables as Mediators of the Association of Acculturation With Sugar-Sweetened Beverage Consumption Among Latinx Adolescents.

The objective of this study was to examine the mediating effects of family support for dietary habits and family meal frequency on the relationship between acculturation and sugar-sweetened beverage (SSB) consumption among Latinx adolescents (N = 131). Acculturation was positively associated with SSB consumption (B = 0.07, P < .01). Results suggest that family support for dietary habits and family meal frequency did not mediate the relationship between acculturation and SSB consumption. However, acculturation was negatively associated with family support for dietary habits (B = -0.10, P < .01) and family meal frequency (B = -0.11, P < .05). Future research should examine other family influences as mediators of the relationship between acculturation and SSB consumption.

Acculturation and sugar-sweetened beverage consumption among Hispanic adolescents: The moderating effect of impulsivity.

Consumption of sugar-sweetened beverages is a risk factor for obesity. Acculturation to the United States (US) might increase sugar-sweetened beverage consumption among Hispanic adolescents, but few moderators of this relationship have been examined. This study examined the moderating influence of impulsivity on the association between acculturation and sugar-sweetened beverages. Hispanic adolescents (n = 154), 14-17 years, were identified and screened for eligibility through low-SES high schools and parents provided consent. Adolescents completed measures of acculturation using Unger's 8-item acculturation scale, impulsivity, and diet. Multiple linear regression was used to examine the main effect of acculturation and the interaction of acculturation with impulsivity on the diet outcomes: sugar-sweetened beverage consumption and percent of calories from sugar. Acculturation was positively associated with sugar-sweetened beverages (ß = 0.43; p < .05). The interaction of acculturation x impulsivity was significant (ß = 0.42, p < .05). Among youth who were more acculturated, those who were more impulsive consumed more sugar-sweetened beverages. Youth who were more acculturated, but less impulsive consumed less sugar-sweetened beverages. Neurocognitive variables such as impulsivity may be important moderators of the influence of acculturation on dietary behavior. Targeted messaging strategies based on levels of acculturation and impulsivity might enhance the effectiveness of interventions designed to reduce the intake of sugar-sweetened beverages among Hispanic adolescents.

Biological, clinical and population relevance of 95 loci for blood lipids.

Plasma concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides are among the most important risk factors for coronary artery disease (CAD) and are targets for therapeutic intervention. We screened the genome for common variants associated with plasma lipids in >100,000 individuals of European ancestry. Here we report 95 significantly associated loci (P < 5 x 10(-8)), with 59 showing genome-wide significant association with lipid traits for the first time. The newly reported associations include single nucleotide polymorphisms (SNPs) near known lipid regulators (for example, CYP7A1, NPC1L1 and SCARB1) as well as in scores of loci not previously implicated in lipoprotein metabolism. The 95 loci contribute not only to normal variation in lipid traits but also to extreme lipid phenotypes and have an impact on lipid traits in three non-European populations (East Asians, South Asians and African Americans). Our results identify several novel loci associated with plasma lipids that are also associated with CAD. Finally, we validated three of the novel genes-GALNT2, PPP1R3B and TTC39B-with experiments in mouse models. Taken together, our findings provide the foundation to develop a broader biological understanding of lipoprotein metabolism and to identify new therapeutic opportunities for the prevention of CAD.

LipidSeq: a next-generation clinical resequencing panel for monogenic dyslipidemias.

We report the design of a targeted resequencing panel for monogenic dyslipidemias, LipidSeq, for the purpose of replacing Sanger sequencing in the clinical detection of dyslipidemia-causing variants. We also evaluate the performance of the LipidSeq approach versus Sanger sequencing in 84 patients with a range of phenotypes including extreme blood lipid concentrations as well as additional dyslipidemias and related metabolic disorders. The panel performs well, with high concordance (95.2%) in samples with known mutations based on Sanger sequencing and a high detection rate (57.9%) of mutations likely to be causative for disease in samples not previously sequenced. Clinical implementation of LipidSeq has the potential to aid in the molecular diagnosis of patients with monogenic dyslipidemias with a high degree of speed and accuracy and at lower cost than either Sanger sequencing or whole exome sequencing. Furthermore, LipidSeq will help to provide a more focused picture of monogenic and polygenic contributors that underlie dyslipidemia while excluding the discovery of incidental pathogenic clinically actionable variants in nonmetabolism-related genes, such as oncogenes, that would otherwise be identified by a whole exome approach, thus minimizing potential ethical issues.

Patient outcomes in canceled MRI-guided breast biopsies.

OBJECTIVE: The reported frequency of aborted MRI-guided breast biopsies ranges from 8% to 17%, usually secondary to nonvisualization at attempted biopsy. Our study examines the frequency of MRI-guided breast biopsies aborted because of lesion nonvisualization and the subsequent risk of malignancy. MATERIALS AND METHODS: We identified 350 patients and 445 lesions scheduled for MRI-guided biopsy between January 1, 2007, and December 31, 2009. Medical records and imaging studies were reviewed to ascertain patient demographics, lesion and imaging characteristics, and subsequent pathology results. Chi-square statistics were calculated for patient level analyses. RESULTS: MRI-guided biopsies were aborted in 13% (56/445) of lesions and 15% (53/350; 95% CI, 11.6-19.3%) of patients because of nonvisualization of the biopsy target at the time of attempted biopsy. Of these 53 patients, 50 patients had follow-up data available. Malignancy was subsequently diagnosed in five of those 50 patients (10%; 95% CI, 3.3-21.8%), three with invasive ductal carcinomas and two with ductal carcinoma in situ. The mean time to malignant diagnosis from the date of aborted biopsy was 2.6 months (range, 1.1-6.9 months). CONCLUSION: Informed consent for MRI-guided breast biopsies should include discussion of biopsy cancellation because of nonvisualization of the target lesion. The low yet significant risk of malignancy in patients subsequent to an aborted MRI-guided breast biopsy warrants short-term follow-up MRI after a canceled biopsy.

Explaining the Correlates of Eating Outside-of-Home Behavior in a Nationally Representative US Sample Using the Multi-Theory Model of Health Behavior Change: A Cross-Sectional Study.

Eating outside-of-home (EOH) is one of the main changes in lifestyle that occurred worldwide in the past few decades. Given that EOH behavior is influenced by individual and contextual factors, the utilization of a theory seems to be suitable in analyzing this health behavior. The fourth-generation theory multi-theory model (MTM) is designed exclusively for health behavior change at the individual and community levels. Therefore, the purpose of this analytical cross-sectional study was to investigate EOH behavior by using the MTM among a nationally representative sample in the United States (US). Data for this study were collected from April-May 2023 via a 61-item psychometric valid, web-based, structured survey disseminated via Qualtrics. Chi-square/Fisher's exact tests were used to compare categorical data, whereas the independent-samples t-test was used to compare the mean scores of MTM constructs across groups. Pearson correlation analysis was performed for the intercorrelation matrix between the MTM constructs and hierarchical regression models were built to predict the variance in the initiation and sustenance by certain predictor variables beyond demographic characteristics. The p values in the multiple comparisons were calculated by using adjusted residuals. Among a total of 532 survey respondents, 397 (74.6%) indicated being engaged in EOH at least twice a week, whereas 135 (25.4%) reported not being engaged in EOH. People who were engaged in EOH were younger (mean age = 42.25 ± 17.78 years vs. 55.89 ± 19.43 years) African American, (15.9% vs. 6.7%, p = 0.01), single or never married, (34.0% vs. 23.0%, p = 0.02), had a graduate degree (9.6% vs. 3.7%, p = 0.03), and were employed (72.0% vs. 34.8%, p < 0.001) as opposed to those who reported not being engaged in eating outside the home. Among the MTM constructs of initiation, "behavioral confidence" and "changes in the physical environment" were the significant predictors of initiating a reduction in EOH behavior and explained 48% of the variance in initiation. Among the MTM constructs of sustenance, "emotional transformation" and "changes in the social environment" were the significant predictors of sustaining a reduction in EOH behavior and explained 50% of the variance in sustenance. This study highlights a need to design MTM-based educational interventions that promote in-home eating instead of frequent EOH for health, family bonding, economic, and other reasons.

Theory-based antecedents of breastfeeding among pregnant women in the United States.

Background: Breastfeeding provides several positive health benefits for the newborn child, yet breastfeeding rates remain low in the United States (US). Theory-based approaches have the potential to improve breastfeeding promotion interventions. Hence, the study examined the correlates of intention to breastfeed among US pregnant women based on the multi-theory model (MTM) of health behavior change. Methods: Using a cross-sectional design, a 36-item online survey was administered to a nationally representative sample of 315 pregnant women in the US. The instrument was psychometrically validated for face, content, and construct validity by a panel of six experts over two rounds. Further, construct validation was done by confirmatory factor analysis (CFA). Hierarchical regression modeling was employed to explain the intention to start breastfeeding and sustain exclusive breastfeeding for up to six months and with complementary foods for up to 24 months. Results: Internal consistency using Cronbach's alpha was found to be acceptable. It was found that behavioral confidence and changes in the physical environment positively affected the initiation of breastfeeding (P<0.01; adjusted R2=0.478). All three constructs of MTM namely practice for change, emotional transformation, and changes in the social environment were significant predictors for the sustenance of breastfeeding at six months (P<0.01; adjusted R2=0.591) and at 24 months (P<0.01; adjusted R2=0.347). Conclusion: Based on the findings of this study it is essential for educators and healthcare providers to design MTM-based interventions to promote breastfeeding among pregnant women in the US.

Allelic and phenotypic spectrum of plasma triglycerides.

The genetic underpinnings of both normal and pathological variation in plasma triglyceride (TG) concentration are relatively well understood compared to many other complex metabolic traits. For instance, genome-wide association studies (GWAS) have revealed 32 common variants that are associated with plasma TG concentrations in healthy epidemiologic populations. Furthermore, GWAS in clinically ascertained hypertriglyceridemia (HTG) patients have shown that almost all of the same TG-raising alleles from epidemiologic samples are also associated with HTG disease status, and that greater accumulation of these alleles reflects the severity of the HTG phenotype. Finally, comprehensive resequencing studies show a burden of rare variants in some of these same genes - namely in LPL, GCKR, APOB and APOA5 - in HTG patients compared to normolipidemic controls. A more complete understanding of the genes and genetic variants associated with plasma TG concentration will enrich our understanding of the molecular pathways that modulate plasma TG metabolism, which may translate into clinical benefit. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease.

Sortilin: an unusual suspect in cholesterol metabolism: from GWAS identification to in vivo biochemical analyses, sortilin has been identified as a novel mediator of human lipoprotein metabolism.

The concentration of low-density lipoprotein (LDL) cholesterol (C) in plasma is a key determinant of cardiovascular disease risk and human genetic studies have long endeavoured to elucidate the pathways that regulate LDL metabolism. Massive genome-wide association studies (GWASs) of common genetic variation associated with LDL-C in the population have implicated SORT1 in LDL metabolism. Using experimental paradigms and standards appropriate for understanding the mechanisms by which common variants alter phenotypic expression, three recent publications have presented divergent and even contradictory findings. Interestingly, although these reports each linked SORT1 to LDL metabolism, they did not agree on a mechanism to explain the association. Here, we review recent mechanistic studies of SORT1 - the first gene identified by GWAS as a determinant of plasma LDL-C to be evaluated mechanistically.

Using the Multi-Theory Model (MTM) of Health Behavior Change to Explain the Seeking of Stool-Based Tests for Colorectal Cancer Screening.

Colorectal cancer is the third most common cancer worldwide and is the second leading cause of cancer-associated deaths. While colorectal cancer is on the decline in the United States (US), disparities still exist, despite the non-invasive screening modalities, such as stool-based tests have shown themselves to be effective in the detection of colorectal cancer. Many of the existing stool-based test interventions lack the use of a contemporary theory-based approach. Given the paucity of theory-based interventions intended to promote stool-based tests, this cross-sectional study utilizes the multi-theory model (MTM) of health behavior change to explain the seeking of stool-based tests for colorectal cancer (CRC) screening. An online 57-item questionnaire with an established psychometric validity was used to collect responses from the US-based sample (n = 640) of adults aged 45-75 years old. The data were analyzed using bivariate and multivariate statistical methods. Structural equation modeling (SEM) was conducted to test the construct validity of the survey instrument. In this nationwide sample, 39.2% (n = 251) of participants reported having received some form of a stool-based test. Among the participants who did not undergo stool-based CRC screening, the MTM subscales, including "participatory dialogue", "behavioral confidence", and "changes in the social environment", were significant predictors of initiating screening behavior and explained 48% of the variance in the initiation among this group (R2 = 0.579, F = 5.916, p < 0.001; adjusted R2 = 0.481). The MTM may be a useful framework with which to design educational, mass media, social media, and clinical interventions for the promotion of stool-based CRC screening among adults aged 45-75 years old.

Lotus japonicus symRK-14 uncouples the cortical and epidermal symbiotic program.

SYMRK is a leucine-rich-repeat (LRR)-receptor kinase that mediates intracellular symbioses of legumes with rhizobia and arbuscular mycorrhizal fungi. It participates in signalling events that lead to epidermal calcium spiking, an early cellular response that is typically considered as central for intracellular accommodation and nodule organogenesis. Here, we describe the Lotus japonicus symRK-14 mutation that alters a conserved GDPC amino-acid sequence in the SYMRK extracellular domain. Normal infection of the epidermis by fungal or bacterial symbionts was aborted in symRK-14. Likewise, epidermal responses of symRK-14 to bacterial signalling, including calcium spiking, NIN gene expression and infection thread formation, were significantly reduced. In contrast, no major negative effects on the formation of nodule primordia and cortical infection were detected. Cumulatively, our data show that the symRK-14 mutation uncouples the epidermal and cortical symbiotic program, while indicating that the SYMRK extracellular domain participates in transduction of non-equivalent signalling events. The GDPC sequence was found to be highly conserved in LRR-receptor kinases in legumes and non-legumes, including the evolutionarily distant bryophytes. Conservation of the GDPC sequence in nearly one-fourth of LRR-receptor-like kinases in the genome of Arabidopsis thaliana suggests, however, that this sequence might also play an important non-symbiotic function in this plant.

Genetic variation in hyaluronan metabolism loci is associated with plasma plasminogen activator inhibitor-1 concentration.

Elevated plasma plasminogen activator inhibitor-1 (PAI-1) concentration is associated with cardiovascular disease risk. PAI-1 is the primary inhibitor of fibrinolysis within both the circulation and the arterial wall, playing roles in both atherosclerosis and thrombosis. To define the heritable component, subjects within the population-based SHARE (Study of Health Assessment and Risk in Ethnic groups) and SHARE-AP (Study of Health Assessment and Risk Evaluation in Aboriginal Peoples) studies, composed of Canadians of South Asian (n = 298), Chinese (n = 284), European (n = 227), and Aboriginal (n = 284) descent, were genotyped using the gene-centric Illumina HumanCVD BeadChip. After imputation, more than 150,000 single nucleotide polymorphisms (SNPs) in more than 2000 loci were tested for association with plasma PAI-1 concentration. Marginal association was observed with the PAI-1 locus itself (SERPINE1; P < .05). However, 5 loci (HABP2, HSPA1A, HYAL1, MBTPS1, TARP) were associated with PAI-1 concentration at a P < 1 × 10(-5) threshold. The protein products of 2 of these loci, hyaluronan binding protein 2 (HABP2) and hyaluronoglucosaminidase 1 (HYAL1), play key roles in hyaluronan metabolism, providing genetic evidence to link these pathways.

The complex genetic basis of plasma triglycerides.

Demonstration of a direct relationship between plasma triglyceride (TG) concentration and atherosclerosis has proven difficult due to confounding variables that accompany elevated plasma TG, such as other dyslipidemias, obesity, and type 2 diabetes. However, human genetic studies have provided evidence suggesting a causal link between plasma TG and cardiovascular risk. Analyses in human patients with hypertriglyceridemia (HTG) also provides insight into the relationship between genetic variation, predisposition to elevated plasma TG, and risk of subsequent cardiovascular disease. Here, we review recent key studies that have contributed to our understanding of the genetic determinants of plasma TG concentration, including HTG susceptibility and phenotypic heterogeneity, and discuss our maturing model of the allelic and phenotypic spectrum of plasma TG.

An increased burden of common and rare lipid-associated risk alleles contributes to the phenotypic spectrum of hypertriglyceridemia.

OBJECTIVE: Earlier studies have suggested that a common genetic architecture underlies the clinically heterogeneous polygenic Fredrickson hyperlipoproteinemia (HLP) phenotypes defined by hypertriglyceridemia (HTG). Here, we comprehensively analyzed 504 HLP-HTG patients and 1213 normotriglyceridemic controls and confirmed that a spectrum of common and rare lipid-associated variants underlies this heterogeneity. METHODS AND RESULTS: First, we demonstrated that genetic determinants of plasma lipids and lipoproteins, including common variants associated with plasma triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) from the Global Lipids Genetics Consortium were associated with multiple HLP-HTG phenotypes. Second, we demonstrated that weighted risk scores composed of common TG-associated variants were distinctly increased across all HLP-HTG phenotypes compared with controls; weighted HDL-C and LDL-C risk scores were also increased, although to a less pronounced degree with some HLP-HTG phenotypes. Interestingly, decomposition of HDL-C and LDL-C risk scores revealed that pleiotropic variants (those jointly associated with TG) accounted for the greatest difference in HDL-C and LDL-C risk scores. The APOE E2/E2 genotype was significantly overrepresented in HLP type 3 versus other phenotypes. Finally, rare variants in 4 genes accumulated equally across HLP-HTG phenotypes. CONCLUSIONS: HTG susceptibility and phenotypic heterogeneity are both influenced by accumulation of common and rare TG-associated variants.

Genetic bases of hypertriglyceridemic phenotypes.

PURPOSE OF REVIEW: Hypertriglyceridemia (HTG) is a common diagnosis. Although secondary factors are important for clinical expression, susceptibility to HTG has a strong genetic component, which we review here. RECENT FINDINGS: Severe HTG in a few families follows Mendelian - typically autosomal recessive - inheritance of rare loss-of-function mutations in genes such as LPL, APOC2, APOA5, LMF1, and GPIHBP1. In contrast, common complex HTG results from the cumulative influence of small-effect variants (single nucleotide polymorphisms) in genes such as APOA5, GCKR, LPL, and APOB. Intensive resequencing of these four genes has also shown accumulated heterozygous rare variants in HTG patients. Together, more than 20% of the susceptibility to HTG is now accounted for by common and rare variants. Further, classical Fredrickson HTG phenotypes, which were once considered to be distinct based on biochemical features, have a shared genetic architecture. SUMMARY: Compared to other complex traits, genetic variants account for a high proportion of HTG diagnoses. By tallying the number of HTG risk alleles, it is possible to discriminate between individuals with HTG and normolipidemia, particularly in those with extreme scores. Future directions include finding the missing genetic component and determining whether genetic profiling can help with diagnosis or personalized treatment advice.

Explaining Correlates of Cervical Cancer Screening among Minority Women in the United States.

Globally, cervical cancer is the fourth leading cause of death among women. While overall cervical cancer rates have decreased over the last few decades, minority women continue to be disproportionately affected compared to White women. Given the paucity of theory-based interventions to promote Pap smear tests among minority women, this cross-sectional study attempts to examine the correlates of cervical cancer screening by Pap test using the Multi-theory Model (MTM) as a theoretical paradigm among minority women in the United States (U.S.). Structural Equation Modelling (SEM) was done for testing the construct validity of the survey instrument. Data were analyzed through bivariate and multivariate tests. In a sample of 364 minority women, nearly 31% (n = 112) of women reported not having received a Pap test within the past three years compared to the national rate (20.8%) for all women. The MTM constructs of participatory dialogue, behavioral confidence, and changes in the physical environment explained a substantial proportion of variance (49.5%) in starting the behavior of getting Pap tests, while the constructs of emotional transformation, practice for change, and changes in the social environment, along with lack of health insurance and annual household income of less than $25,000, significantly explained the variance (73.6%) of the likelihood to sustain the Pap test behavior of getting it every three years. Among those who have had a Pap smear (n = 252), healthcare insurance, emotional transformation, practice for change, and changes in the social environment predicted nearly 83.3% of the variance in sustaining Pap smear test uptake behavior (adjusted R2 = 0.833, F = 45.254, p < 0.001). This study validates the need for health promotion interventions based on MTM to be implemented to address the disparities of lower cervical cancer screenings among minority women.