Where Stories Collide : Montage and the Short Story Cycle

This thesis uses Sergei Eisenstein’s filmic theories of montage to examine the modernist American short story cycle, a genre of independent short stories that work together to create a larger and interrelated whole. Similar to the shot-by-shot editing process of montage, the story cycle builds its intertextual meaning story-by-story from an aggregate of abrupt narrative transitions and juxtapositions. Eisenstein famously felt that montage, the editing together of film fragments, was not a process of linkage, but of collision –each radically different shot in a film should crash into the next shot, until audience members were intellectually provoked into synthesizing these collisions through dialectical processes. I offer montage as an interpretive strategy for negotiating the narrative collisions in story cycles such as Sherwood Anderson’s Winesburg, Ohio, William Faulkner’s Go Down, Moses, and Eudora Welty’s The Golden Apples. For Go Down, Moses, I argue that Eisenstein’s politically rendered “montage of attractions” provides a template for investigating the shock tactics behind Faulkner’s chronologically and racially entangled stories of whites and African Americans. For The Golden Apples, I consider the opposites and doubles in Welty’s fiction with Eisenstein’s similar belief in the “opposing passions” of the world. Not only, then, do I suggest that the modernist story cycle bears a cinematic influence, but I also offer Eisenstein’s theories of montage and collision as a heuristic for formal, thematic, and even political patterns in a genre infamous for its resistance to definition and classification.

Health insurance coverage of Hispanic adults: An assessment of subgroup difference and the impact of immigration

This research explores the health insurance coverage of various Hispanic subgroups in comparison to non-Hispanic whites and blacks. The impact of immigration status is also considered as we hypothesize that nativity, duration, and naturalization tap a possible process of structural acculturation that increases access to insurance coverage for Hispanic groups. We find that the immigration variables impact the type of insurance reported. However, race/ethnic disparities continue to exist, with the various Hispanic subgroups more likely to report miscellaneous government health insurance or no health insurance coverage as compared to non-Hispanic whites.

Toward the Equitable Distribution of Enriching Educational Experiences: Faculty Engagement with Racial Minority Students

Peña, Bensimon, and Colyar (2006) noted: “Not only do African Americans, Hispanics, and Native Americans have lower graduation rates than [do] Whites and Asian Americans, they also experience inequalities in just about every indicator of academic success – from earned grade point average to placement on the dean’s list to graduation rates in competitive majors” (p. 48). While these and other racialized outcomes disparities cannot be attributed to a narrow set of explanatory factors, one thing is known for sure: College students who are actively engaged inside and outside the classroom are considerably more likely than are their disengaged peers to persist through baccalaureate degree attainment. Furthermore, engaged students typically accrue the desired outcomes that are central to liberal education. This is especially true for engagement in what Kuh (2008) refers to as “high-impact” educational experiences – study abroad programs, learning communities, undergraduate research programs, service learning opportunities, and summer internships, to name a few. Unfortunately, racial minority undergraduates are considerably less likely than are their White peers to enjoy the educational benefits associated with these experiences.

Correlates of periodontal decline and biologic markers in older adults

BACKGROUND: There is limited information on infectious and host responses distinguishing older people with or without active periodontitis. This study measured bacterial and serum cytokine and high-sensitivity C-reactive protein (hsCRP) levels in older persons. METHODS: Elders (mean age: 67 years), whose periodontal status had declined most or least (20% worst or 20% best) over 5 years, were enrolled. Two years later, they were classified as periodontally declining (active periodontitis [AP]), if they had at least five teeth with probing depth (PD) > or =5 mm, or stable (stable periodontally [SP]), if they did not. Groups were compared with respect to demographics, PD, clinical loss of attachment, subgingival bacteria, serum hsCRP, interleukin (IL)-1beta and -6, and chronic diseases. RESULTS: Ten AP and 24 SP subjects were identified; 13% of women and 44% of men from the original sample were in the AP group (P <0.05). Most Asians were SP; most whites and all African Americans were classified as having AP (P <0.01). More AP elders had osteoporosis (P <0.01), but the AP and SP groups did not differ with respect to IL-1beta and -6 or hsCRP. Bacterial counts were higher in the AP group for Parvimonas micra (previously Peptostreptococcus micros or Micromonas micros) (7.7 x 10(5) cells versus 3.8 x 10(5) cells; P <0.05), Prevotella intermedia (25.7 x 10(5) cells versus 9.8 x 10(5) cells; P <0.01), Tannerella forsythia (previously T. forsythensis) (16.2 x 10(5) cells versus 8.0 x 10(5) cells; P <0.05), and Streptococcus mutans (6.2 x 10(5) cells versus 2.0 x 10(5) cells; P <0.01). Three risk factors were most predictive of periodontal decline: PD, osteoporosis, and being white or African American. CONCLUSION: Periodontal decline was associated with osteoporosis, ethnicity, PD, gender, serum hsCRP, and levels of four bacterial species.

Hating the neighbors: The role of hate crime in the perpetuation of black residential segregation

Grounded in group conflict theory and the defended neighborhoods thesis, this nationwide empirical study of cities and their residential segregation levels, examines the occurrence of hate crime using data on for all U.S. cities with populations over 95,000, and data compiled from the Uniform Crime Report for hate crime, in conjunction with 2000 census data. Hate crime is any illegal act motivated by pre-formed bias against, in this case, a person’s real or perceived race. This research asks: Do hate crime levels predict white/black segregation levels? How does hate crime predict different measures of white/black segregation? I use the dissimilarity index measure of segregation operationalized as a continuous, binary and ordinal variable, to explore whether hate crime predicts segregation of blacks from whites. In cities with higher rates of hate crime there was higher dissimilarity between whites and blacks, controlling for other factors. The segregation level was more likely to be “high” in a city where hate crime occurred. Blacks are continually multiply disadvantaged and distinctly affected by hate crime and residential segregation. Prior studies of residential segregation have focused almost exclusively on individual choice, residents’ lack of finances, or discriminatory actions that prevent racial minorities from moving, to explore the correlates of segregation. Notably absent from these studies are measures reflecting the level of hate crime occurring in cities. This study demonstrates the importance of considering hate crime and neighborhood conflict when contemplating the causes of residential segregation.

Diversity and function of mutations in p450 oxidoreductase in patients with Antley-Bixler syndrome and disordered steroidogenesis

P450 oxidoreductase (POR) is the obligatory flavoprotein intermediate that transfers electrons from reduced nicotinamide adenine dinucleotide phosphate (NADPH) to all microsomal cytochrome P450 enzymes. Although mouse Por gene ablation causes embryonic lethality, POR missense mutations cause disordered steroidogenesis, ambiguous genitalia, and Antley-Bixler syndrome (ABS), which has also been attributed to fibroblast growth factor receptor 2 (FGFR2) mutations. We sequenced the POR gene and FGFR2 exons 8 and 10 in 32 individuals with ABS and/or hormonal findings that suggested POR deficiency. POR and FGFR2 mutations segregated completely. Fifteen patients carried POR mutations on both alleles, 4 carried mutations on only one allele, 10 carried FGFR2 or FGFR3 mutations, and 3 patients carried no mutations. The 34 affected POR alleles included 10 with A287P (all from whites) and 7 with R457H (four Japanese, one African, two whites); 17 of the 34 alleles carried 16 "private" mutations, including 9 missense and 7 frameshift mutations. These 11 missense mutations, plus 10 others found in databases or reported elsewhere, were recreated by site-directed mutagenesis and were assessed by four assays: reduction of cytochrome c, oxidation of NADPH, support of 17alpha-hydroxylase activity, and support of 17,20 lyase using human P450c17. Assays that were based on cytochrome c, which is not a physiologic substrate for POR, correlated poorly with clinical phenotype, but assays that were based on POR's support of catalysis by P450c17--the enzyme most closely associated with the hormonal phenotype--provided an excellent genotype/phenotype correlation. Our large survey of patients with ABS shows that individuals with an ABS-like phenotype and normal steroidogenesis have FGFR mutations, whereas those with ambiguous genitalia and disordered steroidogenesis should be recognized as having a distinct new disease: POR deficiency.

Influence of Geographical Origin and Ethnicity on Mortality in Patients on Antiretroviral Therapy in Canada, Europe, and the United States

Our objective was to assess differences in all-cause mortality, as well as AIDS and non-AIDS death rates, among patients started on antiretroviral therapy (ART) according to their geographical origin and ethnicity/race in Europe, Canada, and the United States. METHODS: This was a collaboration of 19 cohort studies of human immunodeficiency virus-positive subjects who have initiated ART (ART Cohort Collaboration) between 1998 and 2009. Adjusted mortality hazard ratios (AHRs) were estimated using Cox regression. A competing risk framework was used to estimate adjusted subdistribution hazard ratios for AIDS and non-AIDS mortality. RESULTS: Of 46 648 European patients, 16.3% were from sub-Saharan Africa (SSA), 5.1% Caribbean and Latin America, 1.6% North Africa and Middle East, and 1.7% Asia/West; of 1371 patients from Canada, 14.9% were First Nations and 22.4% migrants, and of 7742 patients from North America, 55.5% were African American and 6.6% Hispanic. Migrants from SSA (AHR, 0.79; 95% confidence interval [CI], .68-.92) and Asia/West (AHR, 0.62; 95% CI, .41-.92) had lower mortality than Europeans; these differences appeared mainly attributable to lower non-AIDS mortality. Compared with white Canadians, mortality in Canadian First Nations people (AHR, 1.48; 95% CI, .96-2.29) was higher, both for AIDS and non-AIDS mortality rates. Among US patients, when compared with whites, African Americans had higher AIDS and non-AIDS mortality, and hazard ratios for all-cause mortality increased with time on ART. CONCLUSIONS: The lower mortality observed in migrants suggests "healthy migrant" effects, whereas the higher mortality in First Nations people and African Americans in North America suggests social inequality gaps. KEYWORDS: HIV infection, antiretroviral therapy, ethnic minorities, migrants Comment in Addressing disparities in HIV mortality: antiretroviral therapy is necessary but not sufficient. [Clin Infect Dis. 2013]

Evaluating the disparity of female breast cancer mortality among racial groups - a spatiotemporal analysis

Background The literature suggests that the distribution of female breast cancer mortality demonstrates spatial concentration. There remains a lack of studies on how the mortality burden may impact racial groups across space and over time. The present study evaluated the geographic variations in breast cancer mortality in Texas females according to three predominant racial groups (non-Hispanic White, Black, and Hispanic females) over a twelve-year period. It sought to clarify whether the spatiotemporal trend might place an uneven burden on particular racial groups, and whether the excess trend has persisted into the current decade. Methods The Spatial Scan Statistic was employed to examine the geographic excess of breast cancer mortality by race in Texas counties between 1990 and 2001. The statistic was conducted with a scan window of a maximum of 90% of the study period and a spatial cluster size of 50% of the population at risk. The next scan was conducted with a purely spatial option to verify whether the excess mortality persisted further. Spatial queries were performed to locate the regions of excess mortality affecting multiple racial groups. Results The first scan identified 4 regions with breast cancer mortality excess in both non-Hispanic White and Hispanic female populations. The most likely excess mortality with a relative risk of 1.12 (p = 0.001) occurred between 1990 and 1996 for non-Hispanic Whites, including 42 Texas counties along Gulf Coast and Central Texas. For Hispanics, West Texas with a relative risk of 1.18 was the most probable region of excess mortality (p = 0.001). Results of the second scan were identical to the first. This suggested that the excess mortality might not persist to the present decade. Spatial queries found that 3 counties in Southeast and 9 counties in Central Texas had excess mortality involving multiple racial groups. Conclusion Spatiotemporal variations in breast cancer mortality affected racial groups at varying levels. There was neither evidence of hot-spot clusters nor persistent spatiotemporal trends of excess mortality into the present decade. Non-Hispanic Whites in the Gulf Coast and Hispanics in West Texas carried the highest burden of mortality, as evidenced by spatial concentration and temporal persistence.

Multiple independent genetic factors at NOS1AP modulate the QT interval in a multi-ethnic population.

Extremes of electrocardiographic QT interval are associated with increased risk for sudden cardiac death (SCD); thus, identification and characterization of genetic variants that modulate QT interval may elucidate the underlying etiology of SCD. Previous studies have revealed an association between a common genetic variant in NOS1AP and QT interval in populations of European ancestry, but this finding has not been extended to other ethnic populations. We sought to characterize the effects of NOS1AP genetic variants on QT interval in the multi-ethnic population-based Dallas Heart Study (DHS, n = 3,072). The SNP most strongly associated with QT interval in previous samples of European ancestry, rs16847548, was the most strongly associated in White (P = 0.005) and Black (P = 3.6 x 10(-5)) participants, with the same direction of effect in Hispanics (P = 0.17), and further showed a significant SNP x sex-interaction (P = 0.03). A second SNP, rs16856785, uncorrelated with rs16847548, was also associated with QT interval in Blacks (P = 0.01), with qualitatively similar results in Whites and Hispanics. In a previously genotyped cohort of 14,107 White individuals drawn from the combined Atherosclerotic Risk in Communities (ARIC) and Cardiovascular Health Study (CHS) cohorts, we validated both the second locus at rs16856785 (P = 7.63 x 10(-8)), as well as the sex-interaction with rs16847548 (P = 8.68 x 10(-6)). These data extend the association of genetic variants in NOS1AP with QT interval to a Black population, with similar trends, though not statistically significant at P<0.05, in Hispanics. In addition, we identify a strong sex-interaction and the presence of a second independent site within NOS1AP associated with the QT interval. These results highlight the consistent and complex role of NOS1AP genetic variants in modulating QT interval.

A spatial-temporal approach to surveillance of prostate cancer disparities in population subgroups

BACKGROUND: Prostate cancer mortality disparities exist among racial/ethnic groups in the United States, yet few studies have explored the spatiotemporal trend of the disease burden. To better understand mortality disparities by geographic regions over time, the present study analyzed the geographic variations of prostate cancer mortality by three Texas racial/ethnic groups over a 22-year period. METHODS: The Spatial Scan Statistic developed by Kulldorff et al was used. Excess mortality was detected using scan windows of 50% and 90% of the study period and a spatial cluster size of 50% of the population at risk. Time trend was analyzed to examine the potential temporal effects of clustering. Spatial queries were used to identify regions with multiple racial/ethnic groups having excess mortality. RESULTS: The most likely area of excess mortality for blacks occurred in Dallas-Metroplex and upper east Texas areas between 1990 and 1999; for Hispanics, in central Texas between 1992 and 1996: and for non-Hispanic whites, in the upper south and west to central Texas areas between 1990 and 1996. Excess mortality persisted among all racial/ethnic groups in the identified counties. The second scan revealed that three counties in west Texas presented an excess mortality for Hispanics from 1980-2001. Many counties bore an excess mortality burden for multiple groups. There is no time trend decline in prostate cancer mortality for blacks and non-Hispanic whites in Texas. CONCLUSION: Disparities in prostate cancer mortality among racial/ethnic groups existed in Texas. Central Texas counties with excess mortality in multiple subgroups warrant further investigation.

Polymorphisms of the DNA repair gene MGMT and risk and progression of head and neck cancer.

Methylating agents are involved in carcinogenesis, and the DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) removes methyl group from O(6)-methylguanine. Genetic variation in DNA repair genes has been shown to contribute to susceptibility to squamous cell carcinoma of the head and neck (SCCHN). We hypothesize that MGMT polymorphisms are associated with risk of SCCHN. In a hospital-based case-control study of 721 patients with SCCHN and 1234 cancer-free controls frequency-matched by age, sex and ethnicity, we genotyped four MGMT polymorphisms, two in exon 3, 16195C>T and 16286C>T and two in the promoter region, 45996G>T and 46346C>A. We found that none of these polymorphisms alone had a significant effect on risk of SCCHN. However, when these four polymorphisms were evaluated together by the number of putative risk genotypes (i.e. 16195CC, 16286CC, 45996GT+TT, and 46346CA+AA), a statistically significantly increased risk of SCCHN was associated with the combined genotypes with three to four risk genotypes, compared with those with zero to two risk genotypes (adjusted odds ratio (OR)=1.27; 95% confidence interval (CI)=1.05-1.53). This increased risk was also more pronounced among young subjects (OR=1.81; 95% CI=1.11-2.96), men (OR=1.24; 95% CI=1.00-1.55), ever smokers (OR=1.25; 95%=1.01-1.56), ever drinkers (OR=1.29; 95% CI=1.04-1.60), patients with oropharyngeal cancer (OR=1.45; 95% CI=1.12-1.87), and oropharyngeal cancer with regional lymph node metastasis (OR=1.52; 95% CI=1.16-1.89). In conclusion, our results suggest that any one of MGMT variants may not have a substantial effect on SCCHN risk, but a joint effect of several MGMT variants may contribute to risk and progression of SCCHN, particularly for oropharyngeal cancer, in non-Hispanic whites.

Ethnic differences in do-not-resuscitate orders after intracerebral hemorrhage.

OBJECTIVE: To explore ethnic differences in do-not-resuscitate orders after intracerebral hemorrhage. DESIGN: Population-based surveillance. SETTING: Corpus Christi, Texas. PATIENTS: All cases of intracerebral hemorrhage in the community of Corpus Christi, TX were ascertained as part of the Brain Attack Surveillance in Corpus Christi (BASIC) project. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Medical records were reviewed for do-not-resuscitate orders. Unadjusted and multivariable logistic regression were used to test for associations between ethnicity and do-not-resuscitate orders, both overall ("any do-not-resuscitate") and within 24 hrs of presentation ("early do-not-resuscitate"), adjusted for age, gender, Glasgow Coma Scale, intracerebral hemorrhage volume, intraventricular hemorrhage, infratentorial hemorrhage, modified Charlson Index, and admission from a nursing home. A total of 270 cases of intracerebral hemorrhage from 2000-2003 were analyzed. Mexican-Americans were younger and had a higher Glasgow Coma Scale than non-Hispanic whites. Mexican-Americans were half as likely as non-Hispanic whites to have early do-not-resuscitate orders in unadjusted analysis (odds ratio 0.45, 95% confidence interval 0.27, 0.75), although this association was not significant when adjusted for age (odds ratio 0.61, 95% confidence interval 0.35, 1.06) and in the fully adjusted model (odds ratio 0.75, 95% confidence interval 0.39, 1.46). Mexican-Americans were less likely than non-Hispanic whites to have do-not-resuscitate orders written at any time point (odds ratio 0.37, 95% confidence interval 0.23, 0.61). Adjustment for age alone attenuated this relationship although it retained significance (odds ratio 0.49, 95% confidence interval 0.29, 0.82). In the fully adjusted model, Mexican-Americans were less likely than non-Hispanic whites to use do-not-resuscitate orders at any time point, although the 95% confidence interval included one (odds ratio 0.52, 95% confidence interval 0.27, 1.00). CONCLUSIONS: Mexican-Americans were less likely than non-Hispanic whites to have do-not-resuscitate orders after intracerebral hemorrhage although the association was attenuated after adjustment for age and other confounders. The persistent trend toward less frequent use of do-not-resuscitate orders in Mexican-Americans suggests that further study is warranted.

The epidemiology of chronic fatigue in San Francisco

Chronic fatigue syndrome (CFS) is a recently defined condition characterized by severe disabling fatigue that persists for a minimum of six months, and a host of somatic and neurocognitive symptoms. Although conditions similar to CFS have been described in the medical literature for over 100 years, little is known about the epidemiology of CFS or of chronic fatigue generally. The San Francisco Fatigue Study was undertaken to describe the prevalence and characteristics of self-reported chronic fatigue and associated conditions in a diverse urban community. The study utilized a cross-sectional telephone survey of a random sample of households in San Francisco, followed by case/control interviews of fatigued and nonfatigued subjects. Respondents were classified as chronically fatigued (CF) if they reported severe fatigue lasting six months or longer, then further classified as having CFS-like illness if, based on self-reported information, their condition appeared to meet CFS case definition criteria. Subjects who reported idiopathic chronic fatigue that did not meet CFS criteria were classified as having ICF-like illness.^ 8004 households were screened, yielding fatigue and demographic information on 16970 residents. CF was reported by 635 persons, 3.7% of the study population. CFS-like illness was identified in 34 subjects (0.2%), and ICF-like illness in 259 subjects (1.6%). Logistic regression analysis indicated that prevalence odds ratios for CFS-like illness were significantly elevated for females compared to males (OR = 2.9), and in Blacks (OR = 2.9) and Native Americans (OR = 13.2) relative to Whites, but significantly lower in Asians (OR = 0.12). Above-average household income was protective for all categories of CF. CFS-like subjects reported more symptoms and were more severely disabled than ICF-like subjects, but the pattern of symptoms experienced by both groups was similar. In conclusion, unexplained chronic fatigue, including CFS-like illness, occurs in all sociodemographic groups, but may be most prevalent among persons with lower incomes and in some racial minorities. Future studies that include clinical evaluation of incident cases of CFS and ICF are required to further clarify the epidemiology of unexplained chronic fatigue in the population. ^

The angiotensin-converting enzyme insertion/deletion polymorphism and its associations with carotid artery wall thickness and coronary heart disease: The atherosclerosis risk in communities study

Coronary heart disease (CHD) is the leading cause of death in the United States. Recently, renin-angiotensin system (RAS) was found associated with atherosclerosis formation, with angiotensin II inducing vascular smooth muscle cell growth and migration, platelet activation and aggregation, and stimulation of plasminogen activator inhibitor-1. Angiotensin II is converted from angiotensin I by angiotensin I-converting enzyme (ACE) and this enzyme is mainly genetically determined. The ACE gene has been assigned to chromosome 17q23 and an insertion/deletion (I/D)polymorphism has been characterized by the presence/absence of a 287 bp fragment in intron 16 of the gene. The two alleles form three genotypes, namely, DD, ID and II and the DD genotype has been linked to higher plasma ACE levels and cell ACE activity.^ In this study, the association between the ACE I/D polymorphism and carotid artery wall thickness measured by B-mode ultrasound was investigated in a biracial sample, and the association between the gene and incident CHD was investigated in whites and if the gene-CHD association in whites, if any, was due to the gene effect on atherosclerosis. The study participants are from the prospective Atherosclerosis Risk in Communities (ARIC) Study, including adults aged 45 to 65 years. The present dissertation used a matched case-control design for studying the associations of the ACE gene with carotid artery atherosclerosis and an unmatched case-control design for the association of the gene with CHD. A significant recessive effect of the D allele on carotid artery thickness was found in blacks (OR = 3.06, 95% C.I: 1.11-8.47, DD vs. ID and II) adjusting for age, gender, cigarette smoking, LDL-cholesterol and diabetes. No similar associations were found in whites. The ACE I/D polymorphism is significantly associated with coronary heart disease in whites, and while stratifying data by carotid artery wall thickness, the significant associations were only observed in thin-walled subgroups. Assuming a recessive effect of the D allele, odds ratio was 2.84 (95% C.I:1.17-6.90, DD vs. ID and II) and it was 2.30 (95% C.I:1.22-4.35, DD vs. ID vs. II) assuming a codominant effect of the D allele. No significant associations were observed while comparing thick-walled CHD cases with thin-walled controls. Following conclusions could be drawn: (1) The ACE I/D polymorphism is unlikely to confer appreciable increase in the risk of carotid atherosclerosis in US whites, but may increases the risk of carotid atherosclerosis in blacks. (2) ACE I/D polymorphism is a genetic risk factor for incident CHD in US whites and this effect is separate from the chronic process of atherosclerosis development. Finally, the associations observed here are not causal, since the I/D polymorphism is in an intron, where no ACE proteins are encoded. ^

A longitudinal comparison of cardiovascular disease risk factors among children and adolescents in the U.S. and Japan: Project HeartBeat!

Blood cholesterol and blood pressure development in childhood and adolescence have important impact on the future adult level of cholesterol and blood pressure, and on increased risk of cardiovascular diseases. The U.S. has higher mortality rates of coronary heart diseases than Japan. A longitudinal comparison in children of risk factor development in the two countries provides more understanding about the causes of cardiovascular disease and its prevention. Such comparisons have not been reported in the past. ^ In Project HeartBeat!, 506 non-Hispanic white, 136 black and 369 Japanese children participated in the study in the U.S. and Japan from 1991 to 1995. A synthetic cohort of ages 8 to 18 years was composed by three cohorts with starting ages at 8, 11, and 14. A multilevel regression model was used for data analysis. ^ The study revealed that the Japanese children had significantly higher slopes of mean total cholesterol (TC) and high density lipoprotein (HDL) cholesterol levels than the U.S. children after adjusting for age and sex. The mean TC level of Japanese children was not significantly different from white and black children. The mean HDL level of Japanese children was significantly higher than white and black children after adjusting for age and sex. The ratio of HDL/TC in Japanese children was significantly higher than in U.S. whites, but not significantly different from the black children. The Japanese group had significantly lower mean diastolic blood pressure phase IV (DBP4) and phase V (DBP5) than the two U.S. groups. The Japanese group also showed significantly higher slopes in systolic blood pressure, DBP5 and DBP4 during the study period than both U.S. groups. The differences were independent from height and body mass index. ^ The study provided the first longitudinal comparison of blood cholesterol and blood pressure between the U.S. and Japanese children and adolescents. It revealed the dynamic process of these factors in the three ethnic groups. ^