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The Communities Advancing Resilience Toolkit (CART)©* is a community-driven, publicly available, theory-based, and evidence-informed community intervention designed to build community resilience to disasters and other adversities. Based on principles of participatory action research, CART applications contribute to community resilience by encouraging and supporting community participation and cooperation, communication, self-awareness, and critical reflection. The primary value of CART lies in its ability to stimulate analysis, collaboration, skill building, resource sharing, and purposeful action. In addition to generating community assessment data, CART can be used as a vehicle for delivering other interventions and creating sustainable capacity within communities. Two models for CART implementation are described.

Background Data-linkage studies have reported an association between congenital anomalies and childhood cancer. However, few studies have focused on the differences in the effect of congenital anomalies on cancer as a function of attained age. We aimed to examine associations between anomalies and childhood cancer as a function of attained age among children born in Oklahoma. Methods Data were obtained from the Oklahoma State Department of Health from 1997 to 2009 (n = 591,235). We linked Vital Statistics records for singleton deliveries to the Oklahoma Birth Defects Registry and the Oklahoma Central Cancer Registry using name and birth date. To assess the relation between anomalies and childhood cancer, we used Cox regression analysis allowing for a nonproportional hazards for anomalies as a function of age. Results There were 23,368 (4.0%) children with anomalies and 531 (0.1%) children with cancer. When considering 3-year age intervals, we detected an increased hazard of any childhood cancer in children with anomalies compared with those without anomalies before 1 year of age (hazard ratio, 14.1; 95% confidence interval, 8.3–23.7) and at 3 years of age (hazard ratio, 2.3; 95% confidence interval, 1.6–3.2). The increased hazard declined with increasing time since birth, with the effect diminished by 6 years of age. Conclusion Our results were consistent with previous studies indicating an increased rate of childhood cancer among children with anomalies at younger ages. Furthermore, our study added a methodological refinement of assessing the effect of anomalies as a function of attained age. Birth Defects Research (Part A), 2016. © 2016 Wiley Periodicals, Inc.

Background Studies comparing serum 25-hydroxyvitamin D concentrations in women with and without polycystic ovary syndrome (PCOS) have produced inconsistent results. Additionally, no previous studies have evaluated associations between vitamin D and specific PCOS phenotypes. Methods This case-control study was conducted among women undergoing intrauterine insemination. Cases (N.=137) were diagnosed with PCOS and then further classified into 3 diagnostic phenotypes based on combinations of the Rotterdam criteria (ovulatory dysfunction+polycystic ovaries [N.=55]; ovulatory dysfunction +androgen excess [N.=15]; and ovulatory dysfunction, +polycystic ovaries, +androgen excess [N.=67]). Controls (N.=103) were ovulatory women without PCOS who were undergoing IUI. Serum total 25-hydroxyvitamin D concentrations were categorized as deficient (≤20 ng/mL), insufficient (21-29 ng/mL), and sufficient (≥30 ng/mL). Prevalence odds ratios (PORs) were calculated using logistic regression. Results A higher proportion (59.9%) of PCOS cases lacked sufficient vitamin D levels compared to controls (47.6%; P value=0.06). The odds of vitamin D deficiency in all PCOS cases were twice that of controls (POR=2.03, 95% CI 0.97-4.26); however, the association was attenuated after adjusting for Body Mass Index (BMI) and race/ethnicity (adjPOR=1.43, 95% CI 0.62, 3.26). When examining PCOS phenotypes exhibiting androgen excess, crude associations were observed for deficient vitamin D levels (unadjPOR=2.93, 95% CI: 1.27, 6.77); however, the association decreased after adjustment for BMI and race/ethnicity (adjPOR=2.03, 95% CI: 0.79, 5.19). Conclusions Vitamin D deficiency occurred more frequently in PCOS cases with androgen excess, but associations were attenuated after adjusting for BMI and race/ethnicity. Combining etiologically distinct PCOS subgroups may obscure associations with lower vitamin D levels and other potential risk factors.

Several atypical antipsychotics (AAPs) are used as second-line agents for treatment resistant depression. AAPs can be expensive compared to other treatment options and can cause several side effects.To estimate healthcare costs and utilization of AAPs compared to other second-line agents.Observational study using Medicaid claims data (2006-2011). Subjects were depression-diagnosed adult members with at least two prescriptions of antidepressant medications followed by a second-line agent. Gamma generalized linear models (GLM) produced estimates of the difference in mean expenditures among treatment groups after adjusting for individual baseline characteristics using propensity scores. Negative binomial models produced estimates of the difference in number of hospitalizations and emergency department (ED) visits.A total of 3910 members received second-line treatment. Treatment groups were AAPs (n = 2211), augmentation agents other than AAPs (n = 1008), and antidepressant switching (n = 691). AAPs resulted in higher mean adjusted pharmacy costs and higher mean adjusted total mental health-related costs. Mean adjusted total healthcare costs and number of inpatient and ED visits were not different among treatments.The results show no evidence that AAPs used as second-line treatment for depression results in overall cost savings or lower inpatient and ED visits compared to other treatment strategies.

Background Unlike various research studies conducted to address dependence among smokers, only a few studies have examined smokeless tobacco (ST) dependence. The Fagerstrom Tolerance Questionnaire (FTQ) and Fagerstrom Test for Nicotine Dependence (FTND) based scales are the most widely used measures of nicotine dependence for both ST users and smokers. These scales were initially developed to measure physical dependence and tolerance and not to assess other salient dimensions of dependence such as craving, compulsion, or withdrawal, as defined by DSM-IV and ICD-10. The aim of this study is to develop and validate a multidimensional scale that has better content coverage, factor structure, and psychometric properties to measure dependence among ST users. Methods 100 adult male smokeless tobacco users were recruited through email distribution lists and community referral. Participants completed three different nicotine dependence questionnaires and provided information related to their tobacco use and demographic characteristics. They also provided a saliva sample for cotinine measurement. In order to develop the new ST scale, subscales and items were selected based on correlation and factor analysis of the modified WISDM-68. Reliability and validity of the new scale, Oklahoma Scale for Smokeless Tobacco Dependence (OSSTD) were also assessed. Results The new ST scale identified seven latent constructs including 23 items to measure ST dependence. Internal consistency as measured by Cronbach's coefficient (α = 0.925) indicated better reliability of OSSTD than FTND-ST. Concurrent validity of OSSTD as evaluated by comparing it with dependence diagnosis and FTND-ST was affirmative. There was a significant correlation between the OSSTD total score and the cotinine levels and tobacco use characteristics among study participants. Conclusion OSSTD possesses better psychometric properties and provides an effective and efficient tool to measure ST dependence as a multidimensional construct.

Although the majority of smokers attempting to quit do so without assistance, research in the area of unassisted quit behaviors is limited. The aim of this study was to investigate whether population-level policies and programs, such as smoke-free air policies and tobacco control programs, contribute to unassisted quit attempts and cessation.The current study used the 2003 Tobacco Use Supplement to the Current Population Survey (TUS-CPS) special Cessation Supplement (CS) to estimate unassisted quit attempt and success rates by state. Linear regression was used to examine whether state-level unassisted quit attempt and success rates were related to state-level policies and social norms. State-level factors investigated were tobacco control program funding, tobacco taxes, smoke-free air policies, state anti-smoking sentiment and recent change in smoking prevalence.Consistent with previous studies, this study found the majority of smokers who attempted to quit did so without assistance. This study also found unassisted quit attempt rates were higher than assisted attempt rates in every state and DC. Additionally, unassisted quit success rates were higher than assisted quit success rates in most states; however, some states had higher assisted quit success rates. State-level factors associated with unassisted quit attempt rates included anti-smoking sentiment and tobacco taxes; however, no significant relationships were uncovered between unassisted quit success rates and state-level factors.These results suggest that state-level factors may be more important in motivating smokers to attempt quitting, and other individual factors or unmeasured state factors may be related to quit success.

Objective: To describe the epidemiology of ADHD in communities using a DSM-IVTR case definition. Method: This community-based study used multiple informants to develop and apply a DSM -IVTR-based case definition of ADHD to screening and diagnostic interview data collected for children 5-13 years of age. Teachers screened 10,427 children (66.4%) in four school districts across two states (SC and OK). ADHD ratings by teachers and parent reports of diagnosis and medication treatment were used to stratify children into high and low risk for ADHD. Parents (n = 855) of high risk and gender frequency-matched low risk children completed structured diagnostic interviews. The case definition was applied to generate community prevalence estimates, weighted to reflect the complex sampling design. Results: ADHD prevalence was 8.7% in SC and 10.6% in OK. The prevalence of ADHD medication use was 10.1% (SC) and 7.4% (OK). Of those medicated, 39.5% (SC) and 28.3% (OK) met the case definition. Comparison children taking medication had higher mean symptom counts than other comparison children. Conclusions: Our ADHD estimates are at the upper end of those from previous studies. The identification of a large proportion of comparison children taking ADHD medication suggests that our estimates may be conservative; these children were not included as cases in the case definition, although some might be effectively treated.

The purpose of this pilot randomized controlled study was to identify any effects of power wheelchairs on the development and function of young children with severe motor impairments.Participants were 28 children with various diagnoses, aged 14 to 30 months when they entered the study. The Battelle Developmental Inventory (BDI), Pediatric Evaluation of Disability Inventory, and Early Coping Inventory were administered at entry and after 12 months.The on-protocol analysis comparing median change scores showed the experimental groups' BDI receptive communication scores, and their Pediatric Evaluation of Disability Inventory mobility functional skills, mobility caregiver assistance, and self-care caregiver scores improved significantly more than the control group's scores. An intention-to-treat analysis upheld the findings and revealed an additional difference between the groups' BDI total score.The results support use of power wheelchairs with children as young as age 14 months to enhance development and function, although additional research is needed.

Aims: This study demonstrates that auxiliary and exclusion criteria variables increase the effectiveness of missing imputation in correcting underestimation of physiologic reactivity in relation to post-traumatic stress disorder (PTSD) caused by deleting cases with missing physiologic data. Methods: This study used data from survivors of the 1995 Oklahoma City bombing and imputed missing heart rate data using auxiliary and exclusion criteria variables. Logistic regression was used to examine heart rate reactivity in relation to current PTSD. Results: Of 113 survivors who participated in the bombing study's 7-year follow-up interview, 42 (37%) had missing data on heart rate reactivity due to exclusion criteria (medical illness or use of cardiovascular or psychotropic medications) or non-participation. Logistic regression results based on imputed heart rate data using exclusion criteria and auxiliary (the presence of any current PTSD arousal symptoms) variables showed that survivors with current bombing-related PTSD had significantly higher heart rates at baseline and recovered more slowly back to baseline heart rate during resting periods than survivors without current PTSD, while results based on complete cases failed to show significant correlations between current PTSD and heart rates at any assessment points. Conclusions: Suggested methods yielded an otherwise undetectable link between physiology and current PTSD.

BACKGROUND:: Whether severely injured patients should be transported directly to tertiary trauma centers, bypassing closer nontertiary facilities, or be transported first to nearby, less-specialized facilities for immediate care and stabilization has been studied with mixed findings. Differences in study locale, case mix, and variation in the structure and level of maturation of the trauma system may explain some of the discrepancy in findings. In addition, risk adjustment strategies used in these studies did not take into account prehospital baseline characteristics as well as time since injury. METHODS:: This was a retrospective cohort study of 1,998 patients treated at a Level I trauma center between January 1, 2006, and December 31, 2007. Propensity-adjusted survival analyses were used to compare short-term mortality outcomes in transferred versus directly transported major trauma patients. RESULTS:: A total of 1,398 patients were transported directly to the Level I trauma center and 600 patients were transferred from lower level facilities. After adjusting for the propensity to be transported directly, age, injury severity score, severe head injury, emergency medical service or emergency department intubation, comorbid conditions, and time to definitive Level I trauma care, the 2-week mortality risk in transferred patients was almost three-fold that of patients transported directly to a Level I trauma center (hazard ratio, 2.7; 95% confidence interval, 1.31-5.6). CONCLUSION:: Transferred patients in a predominantly rural region are at an increased risk of short-term mortality. This suggests that severely injured patients should be transported directly to tertiary trauma centers. For patients requiring immediate stabilization at nontertiary facilities, this should be performed promptly without unnecessary delays. Language: en

Objectives: Recent evidence suggests a measurable reduction in mortality for patients transferred from a nontertiary trauma center (Level III or IV) to a Level I trauma center, but not for those transferred to a Level II trauma center. Whether this can be generalized to a predominantly rural region with fewer tertiary trauma care resources is uncertain. This study sought to evaluate mortality differences for patients initially presenting to nontertiary trauma centers in a predominantly rural region depending on transfer status. Methods: This was a retrospective cohort study of patients initially presenting to 104 nontertiary trauma centers in Oklahoma and meeting the state’s criteria for major trauma. Patients dying within 1 hour of emergency department (ED) arrival at the nontertiary trauma center were excluded. The exposure variable of interest was admission status, which was categorized as either transfer to a tertiary (Level I or II) trauma center within 24 hours or admission to a nontertiary trauma center. Propensity scores were used to minimize the selection bias inherent in the decision to admit or transfer a patient for higher-level care. Multiple logistic regression was used to generate three propensity score models: probability of transfer to either a Level I or II, Level I only, and Level II only. Propensity scores were then included as a covariate in multivariable Cox regression models assessing outcome differences between admitted and transferred patients. The outcome of interest was 30-day mortality, defined as death at either the nontertiary trauma center or the tertiary trauma center within 30 days of arrival at the initial Level III/IV center’s ED. Results: A total of 6,229 patients met study criteria, of whom 2,669 (43%) were transferred to tertiary trauma centers. Of those transferred, 1,422 patients (53%) were transferred to a Level I trauma center. Crude mortality was lower for patients transferred to tertiary trauma centers compared to those remaining at nontertiary trauma facilities (hazard ratio [HR] = 0.59; 95% confidence interval [CI] = 0.48 to 0.72). After adjusting for the propensity to be transferred, Injury Severity Score (ISS), presence of severe head injury, and age, transfer to a tertiary trauma center was associated with a significantly lower 30-day mortality (HR = 0.38; 95% CI = 0.30 to 0.50) compared to admission and treatment at a nontertiary trauma center. The observed survival benefit was similar for patients transferred to a Level I trauma center (HR = 0.36; 95% CI = 0.20 to 0.4) and those transferred to a Level II center (HR = 0.45; 95% CI = 0.33 to 0.61). Conclusions: This study suggests a survival benefit among patients initially presenting to nontertiary trauma centers who are subsequently transferred to tertiary trauma centers compared to those remaining in nontertiary trauma centers, even after adjusting for variables affecting the likelihood of transfer. Although this survival benefit was larger for patients treated at a Level I trauma center, Level II trauma centers in a region with few tertiary trauma resources demonstrated a measurable benefit as well. ACADEMIC EMERGENCY MEDICINE 2010; 17:1223–1232 © 2010 by the Society for Academic Emergency Medicine

Troponin I Levels After Spontaneous ICD Shocks.Introduction: Serum cardiac troponin I (cTnI) is a sensitive and specific marker for myocardial injury. Myocardial ischemia and/or injury can be a trigger for ventricular arrhythmias. The aim of this study was to assess the frequency and significance of elevated serum cTnI levels after spontaneous implantable cardioverter defibrillator (ICD) shocks. Methods and Results: Serial cTnI measurements and ECGs were performed in 35 patients with transvenous ICDs who were admitted after spontaneous ICD shocks. Elevated cTnI levels were found in 18 patients (51%). Acute coronary syndrome was diagnosed in 5 (22%) of 23 patients with known coronary artery disease. After excluding the patients with acute coronary syndrome, elevated cTnI levels were present in 13 (43%) of 30 patients: 18% of patients with 3 shocks. Patients with elevated cTnI levels received a higher number of shocks (16 ± 18 vs 5 ± 7; P < 0.05) and had higher total delivered energies (475 ± 538 J vs 128 ± 184 J; P < 0.05) compared with patients with normal cTnI. Patients with acute coronary syndrome had higher peak cTnI levels (18 ± 16 ng/mL) compared with patients with elevated cTnI without acute coronary syndrome (3.8 ± 4.3 ng/mL; P < 0.01). Conclusion: Serum cTnI rises occur in the majority of patients after multiple (> 3) spontaneous ICD discharges but are due to acute coronary syndrome only 14% of the time (22% of the time in patients with known coronary artery disease).

Autoantibodies to the 20-kDa ribosomal proteins (L12/S10) are not well studied, especially in juveniles with systemic lupus erythematosus (SLE). Randomly selected sera from American juveniles and adults with SLE were screened for antibodies to either 20-kDa protein and P proteins and then assayed for anti-L12 and anti-S10 by immunoblot assays. In a pilot study of patients with anti-P (Cohort 1), IgG antibodies to either 20-kDa protein and, specifically, to L12 were observed in 72 and 42% of juveniles and adults, respectively. IgG antibodies to S10 were detected less frequently. In Cohort 2 patients who were chosen irrespective of autoantibody status, twice as many juveniles as adults had IgG antibodies to either 20-kDa protein. Prevalences of IgG anti-L12 and IgG anti-S10 antibodies in the juveniles were 28 and 16% and in the adults were 13 and 12%, respectively. Anti-L12 were strongly but not invariably associated with anti-P, and usually arose temporally to these antibodies. Anti-S10 activity was due to anti-Sm antibodies. We conclude that IgG anti-L12 are more prevalent in SLE than previously reported, and are responsible for the majority of activity toward the 20-kDa ribosomal proteins, especially in juveniles.

Objective The possible molecular mimicry of the Epstein-Barr virus (EBV) peptide PPPGRRP by the peptide PPPGMRPP from Sm B'/B of the human spliceosome is consistent with the possibility that EBV infection is related to the origin of systemic lupus erythematosus (SLE) in some patients. Association of EBV exposure with SLE was therefore tested for and subsequently found in children and adolescents (odds ratio [OR] 49.9, 95% confidence interval [95% CI] 9.3-1,025, P 10, 95% CI 2.53-infinity, P Methods We selected 196 antinuclear antibody-positive adult SLE patients (age > or =20 years) and 2 age-, race-, and sex-matched controls per patient. SLE patients and matched controls were tested for evidence of previous infection with EBV, cytomegalovirus (CMV), herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), or varicella-zoster virus (VZV) by standardized enzyme-linked immunosorbent assays. Results Of the 196 lupus patients tested, all but 1 had been exposed to EBV, while 22 of the 392 controls did not have antibodies consistent with previous EBV exposure (OR 9.35, 95% CI 1.45-infinity, P = 0.014). No differences were observed between SLE patients and controls in the seroconversion rate against CMV, HSV-2, or VZV. Conclusion These new data from adults, along with the many suggestive features of EBV infection, are consistent with the contribution of this infection to the etiology of SLE.

The authors describe the development and evaluation of a continuing education program in biostatistics and epidemiology. Short courses were presented to public health and mental health professionals using teaching strategies that included lecture, discussion, practice-oriented examples, and interactive problem-solving. A total of 1723 health professionals attended one or more of the 120 courses presented from 1992 to 1996 in seven US states. Most course participants were female: the highest education level for 40% was a bachelor's degree, while 42% had advanced degrees. Approximately 66% of participants signed up for continuing education credits. The program represents a successful partnership between an academic institution and health agencies in a seven-state region.

Objective Genetic susceptibility to systemic lupus erythematosus (SLE) is undoubtedly complex and, presumably, involves multiple loci. Linkage of SLE to D1S229 at chromosome 1q41 has been previously reported in a cohort of 52 affected sibpairs. The present study sought to confirm this reported linkage in an independent cohort of 127 extended multiplex SLE pedigrees containing 107 affected sibpairs. Methods Genotype data were collected for D1S229 and 18 flanking microsatellite markers spanning chromosome 1q32–1q42. Analyses of genotype data included a model-based logarithm of odds (LOD) score approach, affected sibpair analyses, and transmission disequilibrium tests. Results A maximum LOD score of 1.46 was found with D1S229 in a subgroup of 78 European American pedigrees, with additional support from multiple markers clustered around D1S229. Increased allele sharing in affected siblings was most significant at D1S2616, particularly in European Americans (P = 0.0005), followed by D1S229 (P = 0.002), D1S490 (P = 0.028), and D1S1605 (P = 0.037). Although linkage in a subgroup of 40 African American pedigrees was not suggested by the analyses of any marker tested in the chromosomal region surrounding D1S229, a maximum LOD score of 3.03 was found with D1S3462, mapped 15 centimorgans distal to D1S229. Conclusion Our linkage analysis results in European Americans at D1S229 are remarkably similar to those previously reported. That at least 1 genetic effect near this locus is important for susceptibility to lupus should now be generally accepted, and efforts to identify the gene are thereby justified.

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by production of autoantibodies against intracellular antigens including DNA, ribosomal P, Ro (SS-A), La (SS-B), and the spliceosome. Etiology is suspected to involve genetic and environmental factors. Evidence of genetic involvement includes: associations with HLA-DR3, HLA-DR2, Fcγ receptors (FcγR) IIA and IIIA, and hereditary complement component deficiencies, as well as familial aggregation, monozygotic twin concordance >20%, λ s > 10, purported linkage at 1q41–42, and inbred mouse strains that consistently develop lupus. We have completed a genome scan in 94 extended multiplex pedigrees by using model-based linkage analysis. Potential [log 10 of the odds for linkage (lod) > 2.0] SLE loci have been identified at chromosomes 1q41, 1q23, and 11q14–23 in African-Americans; 14q11, 4p15, 11q25, 2q32, 19q13, 6q26–27, and 12p12–11 in European-Americans; and 1q23, 13q32, 20q13, and 1q31 in all pedigrees combined. An effect for the FcγRIIA candidate polymorphism) at 1q23 (lod = 3.37 in African-Americans) is syntenic with linkage in a murine model of lupus. Sib-pair and multipoint nonparametric analyses also support linkage ( P < 0.05) at nine loci detected by using two-point lod score analysis (lod > 2.0). Our results are consistent with the presumed complexity of genetic susceptibility to SLE and illustrate racial origin is likely to influence the specific nature of these genetic effects.

Autoantibodies to anti-ribosomal P protein have been recognized in patients with systemic lupus erythematosus (SLE) in widely variable proportions of unselected patients. Presence of anti-ribosomal P antibodies was retrospectively studied in 69 patients with SLE during disease exacerbations and remissions or during continuously active disease. Anti-ribosomal P antibodies were positive in 21/69 patients during active disease, with an overall prevalence of 30.4%. Prevalence in patients with active nephritis was 75.0% (15/20), P value by Fisher's exact test of 8.39 × 10 −7 . In 12/13 patients (92.3%), anti-P disappeared during periods of disease remission, P = 0.0002. In 17/21 patients (81.0%) with anti-ribosomal P antibodies, anti-dsDNA antibodies were also positive. In 47 patients without anti-P, 23/47 (48.9%) were also positive for anti-dsDNA. In 9/12 patients (75.0%) titers of anti-dsDNA antibodies correlated with anti-P during disease exacerbations and remissions, P = 0.004. The higher prevalence of anti-P in patients with lupus nephritis with disappearance during disease remissions supports the hypothesis of an immunopathogenetic role of these antibodies in lupus nephritis. There was also a strong association between anti-dsDNA and anti-P antibodies.

Objective. To determine if antiribosomal P (anti-P) autoantibodies are present in healthy children. Methods. Sera from healthy children were screened for anti-P by conventional enzyme-linked immunosorbent assay and immunoblot techniques. Sera were also treated with immobilized ribosomal P antigens on nitrocellulose strips; affinity-purified fractions were tested for anti-P by high-sensitivity immunoblot. The relative binding affinities were compared for affinity-purified anti-P antibodies from healthy children and adults, and patients with systemic lupus erythematosus. IgG fractions of anti-P-depleted sera from healthy children were assessed for inhibition of autolo-gous anti-P activity. Results. Conventional serologic screening showed no IgG nor IgM anti-P in 88 untreated sera. IgG anti-P were unmasked in all 79 sera treated by the membrane batch affinity technique. IgM anti-P were identified in 27 of the treated sera; the percentage of positive sera decreased with increasing age (X 2 for linear trend P = 0.00081). Affinity-purified anti-P from children had relative binding affinities similar to those of anti-P from other groups. Sera from healthy children contained inhibitory IgG antibodies to anti-P. Conclusion. These results show that anti-P autoantibodies are present in all healthy children. The majority of these autoantibodies are masked by IgG antibodies, suggesting concordant development of a regulatory network.

SUMMARY Patients with systemic lupus erythematosus (SLE) frequently have anti-lymphocyte autoantibodies, some of which also bind to surfaces of neurons. Since anti-ribosomal P protein autoantibodies (anti-P) from SLE patients also bind to surfaces of neurons, we hypothesized that anti-P are anti-lymphocyte antibodies. A panel of human T lymphocytes was evaluated for anti-P binding by indirect immunofluorescence. Affinity-purified anti-ribosomal antibodies were used as a source of anti-P. These autoantibodies bound to the surfaces of all transformed T cell lines tested. This binding was not mediated by Fc receptors. It was inhibitable by ribosomes. Anti-P bound to circulating T lymphocytes from healthy adults and children. They also bound to thymocytes and cord blood T cells from normal neonates. Circulating T cells from SLE patients with anti-P bound less anti-P than cells from healthy controls. Two patients were studied on multiple occasions. The capacity of their T cells to bind anti-P correlated inversely with titres of anti-ribosomal antibodies. Anti-ribosomal antibodies, other than anti-P, also appear to bind to T cells. The surface of T cells contains a protein with the size and antigenicity of the ribosomal P protein, P0. We conclude that anti-ribosomal antibodies are a subset of anti-lymphocyte autoantibodies. Their possible role in the pathogenesis of lymphopenia or lymphocyte dysfunction in SLE has to be defined in further studies.

While building community resilience to disasters is becoming an important strategy in emergency management, this is a new field of research with few available instruments for assessing community resilience. This article describes the development of the Communities Advancing Resilience Toolkit (CART) survey instrument. CART is a community intervention designed to enhance community resilience to disasters, in part, by engaging communities in measuring it. The survey instrument, originally based on community capacity and related literature and on key informant input, was refined through a series of four field tests. Community organizations worked with researchers in a participatory action process that provided access to samples and helped to guide the research. Exploratory factor analysis performed after each field test led to the identification of four interrelated constructs (also called domains) which represent the foundation for CART Connection and Caring, Resources, Transformative Potential, and Disaster Management. This model was confirmed using confirmatory factor analysis on two community samples. The CART survey can provide data for organizations and communities interested in assessing a community's resilience to disasters. Baseline data, preferably collected pre disaster can be compared to data collected post disaster and/or post intervention.

This study examined the psychometric properties of the Vanderbilt AD/HD Diagnostic Teacher Rating Scale (VADTRS).Information was collected from teachers and parents in 5 school districts (urban, suburban, and rural). All teachers in participating schools were asked to complete the VADTRS on all their students. Construct validity was evaluated through an exploratory factor analysis investigation of the 35 items that made up the 4 scales of inattention, hyperactivity, conduct/oppositional problems, and anxiety/depression problems. Convergent validity was assessed among a subsample of participants whose teachers completed the Strengths and Difficulties Questionnaire (SDQ). Finally, predictive validity was examined for another subsample of high- and low-risk children whose parents completed a structured psychiatric interview, the Diagnostic Interview Schedule for Children-IV.For construct validity, a 4-factor model (inattention, hyperactivity, conduct/oppositional, and anxiety/depression problems) fits the data well. The estimates of the KR20 coefficient for a binary item version of the scale ranged from .85 to .94. Convergent validity with the SDQ was high (Pearson's correlations.72) for these 4 factors. For predictive validity, the VADTRS produced a sensitivity of .69, specificity of .84, positive predictive value of .32, and negative predictive value of .96 when predicting future case definitions among children whose parents completed a diagnostic interview.The confirmation of the construct and convergent validity and acceptable scale reliabilities found in this study further supports the utility of the VADTRS as a diagnostic rating scale for attention-deficit hyperactivity disorder. The low predictive validity further demonstrates the need for multiple observers in establishing the diagnosis.

The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT) or electronic cigarettes (EC). Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31), as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001). The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption.

A nonparametric method for linkage analysis has been developed and applied to the Problem 1 data set of the Genetic Analysis Workshop 9. Basically, the univariate matched pair strategy of the transmission disequilibrium test has been adapted to multivariate modeling using the conditional logistic function. After setting the critical value for significance at p ⩽ 0.0001, models at only D5G23 and D1G31 appear to be significant (p < 10−7). Logistic transmission modeling is a powerful method for establishing linkage by disequilibrium. ©1995 Wiley-Liss, Inc.

Diverse clinical presentations of SLE create significant diagnostic difficulties. However, the common feature of autoantibodies has been shown to associate with select clinical features (1). Previous work has found that autoantibodies are often present in SLE patient sera years before diagnosis and prior to their associated clinical symptoms (2, 3). Detection of autoantibodies contributes to SLE classification (4, 5), and some may be used to monitor the potential for disease flare (6, 7). Prevalence of autoantibodies varies among self-reported ethnic groups. Compared with European-Americans (EA), African-American (AA) SLE patients have a higher prevalence of autoantibodies targeting Sm and nRNP proteins (8–11). Autoantibody cluster analysis provides additional information about clinical symptom associations or genetic risk; however, studies to date have either relatively small patient cohorts (12–15) or use historical antibody data measured by a variety of detection methods (16). A few studies examining the prevalence of autoantibodies in blood relatives of SLE patients have shown that low levels of SLE specific autoantibodies were detectable in clinically healthy relatives (17–19). Although autoantibodies remain paramount in lupus diagnosis and management, detection of lupus specificities vary significantly between clinically available assays. To date, detailed evaluations of newer methodologies in large multi-ethnic SLE and control collections are incomplete. Historical methods of immunofluorescence and immunodiffusion autoantibody testing require specially trained laboratory personnel and are becoming less available in many US markets. Based on variability in autoantibody detection across and within select methods, it has been difficult to consistently and accurately measure prevalence of autoantibodies in diverse SLE patient cohorts. Questions remain about the number of SLE patients that would be potentially missed based upon testing of fewer autoantibody specificities with newer methodologies; the frequency of specific autoantibody detection across different races; and if healthy SLE family members would have higher rates of autoantibody specificities when using these newer methods. Our primary objective was to examine prevalence, specificity, clustering and family aggregation of specific autoantibodies within a large cohort of SLE patients, unaffected relatives, and unaffected controls. Additionally, we sought to compare anti-nuclear antibody (ANA) results between a multiplex bead assay and classical detection methods (indirect immunofluorescence and immunodiffusion) in a large multi-ethnic cohort.

To determine the prevalence of immune thrombocytopenia (ITP) in Oklahoma regardless of age, clinical characteristics, insurance status, and source of health care. Patients with ITP were identified by the administrative code ICD-9-CM 287.3 in Oklahoma hematologists' offices for a 2-year period, 2003–2004. Prevalence was estimated separately for children (

Background Undertriage of elderly trauma patients to tertiary trauma centers is well documented. This study evaluated the impact of directness of transport to a Level I trauma center on morbidity in geriatric trauma patients sustaining severe pelvic fractures. Methods This was a retrospective cohort study of 87 geriatric trauma patients diagnosed with potentially unstable pelvic fractures, treated at a Level I trauma center between 2008 and 2010. Results Of the 87 patients, 39% (34 of 87) initially were transported to a nontertiary trauma center. After adjusting for presence of comorbidity and injury severity, the 2-week incidence of complications was 54% higher in transferred patients compared with those directly transported (rate ratio, 1.54; 95% confidence interval, .95–2.54). In particular, transferred patients had increased odds of developing pneumonia/systemic inflammatory response syndrome. Conclusions Despite lacking precision, results of this study suggest an increased risk of complications in transferred geriatric trauma patients with severe pelvic fractures compared with their directly transported counterparts.

A mathematical analysis shows how the magnitude of the correlation coefficient increases with the range over which linearly related variables are measured. This dependence should be taken into account when comparing correlation coefficients. Our treatment is applied here to comparisons of rainfall estimated by radar and raingage. The magnitude of the coefficient of correlation between measures of the same quantity by different processes is defined by an equation that accounts for standard errors of estimates, the range of values, and the density distribution function. We present one equation for uniform densities of variables and another for densities inversely proportional to magnitude. The latter density distribution corresponds to raw rainfall data and the former to logarithms of the same data.

B lymphocyte stimulator (BLyS, also known as TNFSF13B and BAFF) is a type II transmembrane protein and a member of the TNF superfamily (1, 2). BLyS is produced by several different cell types, including monocytes, activated neutrophils, T cells, and dendritic cells (3–5), and is expressed as a cell surface protein which can be furin-cleaved and released into the circulation. Although BLyS has been shown to be constitutively expressed, certain inflammatory cytokines such as IL-2, TNF-α, IFN-γ, and IFN-α can enhance its production and secretion (3, 4, 6, 7). BLyS binds to 3 receptors found primarily on B cells (8). Activation of these receptors leads to B cell proliferation, differentiation, survival, and IgG class switching (1, 4, 9). BLyS has been shown to play an important role in primary immune responses, as anti-BLyS treated mice show profoundly reduced numbers of naive B cells with accompanying attenuated responses to both T-dependent and T-independent antigens (10). Transgenic mice that overexpress BLyS display a myriad of autoimmune features, such as high levels of rheumatoid factor, anti-DNA, circulating immune complexes, and immunoglobulin deposition in the kidneys (9). Mice treated with exogenous BLyS develop an increase in B cell numbers, particularly those directed against chromatin (11), and autoreactive cells encountering transitional B cell checkpoints in the spleen require higher concentrations of BLyS to survive than do non-autoreactive B cells (8, 9, 12). Mouse models have also demonstrated that deletion of either BLyS or its receptor severely impairs B cell development beyond the transitional stage with a resulting decrease in peripheral B cell populations (9, 13–15). Elevated circulating BLyS levels have been found in patients with systemic autoimmune disorders such as SLE, rheumatoid arthritis (RA), and Sjoren’s syndrome (16–18). Early reports found increased serum BLyS levels in SLE patients compared to healthy individuals that correlated with anti-dsDNA titers, but not disease activity (16, 17, 19). BLyS levels did, however, decrease following high-dose corticosteroid treatment (19). Other studies found that peripheral blood leukocyte BLyS mRNA levels correlated with SLE disease activity (20, 21). While most of these initial studies, which were performed in mainly Hispanic SLE patients, failed to demonstrate a correlation between serum BLyS levels and disease activity, a later longitudinal study undertaken at 4 different clinical centers that contained ancestral diversity, found an association between increases in plasma BLyS levels from a previous visit and increases in SELENA-SLEDAI scores at the next visit (22). Additionally, another study involving Norwegian SLE patients, also found a correlation with serum BLyS levels and SLEDAI scores (23). A study examining plasma BLyS protein levels in pediatric SLE also demonstrated an association between elevated BLyS levels and increased disease activity (24). IFN-α has proven to be a key cytokine in SLE pathogenesis, and has been shown to increase BLyS expression in antigen-presenting cells (4). Therefore, it is possible that IFN-α plays a role in driving BLyS production in SLE, although a direct correlation between circulating BLyS levels and serum IFN-α activity has yet to be demonstrated in SLE patients. Additionally, several environmental factors have been implicated in the pathogenesis of SLE (25), including vitamin D deficiency (26). As vitamin D has been shown to suppress the expression of the IFN signature in myeloid-derived dendritic cells, as well as suppress B cell activation and immunoglobulin production (27, 28), it is of interest to assess the relationship between vitamin D and BLyS levels. Belimumab is a fully human monoclonal antibody that binds BLyS and inhibits its activity. Two recent large randomized, double-blind, placebo-controlled, multicenter phase 3 trials, BLISS-52 and BLISS-76, evaluated the efficacy of belimumab plus standard of care compared to placebo plus standard of care; positive results were obtained with both studies reaching their primary efficacy endpoints of reductions in disease activity without ancillary organ flares (29, 30). Taken together, these data suggest that excessive BLyS may be an important mechanism underlying SLE pathogenesis and that BLyS targeted therapies seem promising. However, normal B cell function requires some BLyS activity. To date no studies have evaluated whether specific levels of BLyS are required to mount appropriate vaccination responses or whether BLyS levels change after vaccination. The primary objective of this study is to investigate the relationship between circulating BLyS levels and humoral responses made to influenza vaccination, as well as the effect of influenza vaccination on BLyS production in SLE. The current study also examines select demographic, environmental, and clinical features of SLE for association with elevated BLyS levels in an effort to better understand the mechanisms of elevated BLyS in a heterogeneous SLE population.

BACKGROUND:: Indications for direct transport may be strongly related to risk of future health outcomes, and these indications may not be adequately controlled by considering only in-hospital variables. This study was designed to identify prehospital factors associated with directness of transport. METHODS:: The study included 2,062 patients treated at a Level I trauma center between January 1, 2006, and December 31, 2007. The outcome of interest was directness of transport to a Level I trauma center. A propensity score analysis was used to identify demographic, clinical, distance, and other injury scene-related variables associated with the probability of direct transport. RESULTS:: A total of 1,459 patients were directly transported to the Level I trauma center and 603 were transferred from lower level facilities. Patients were more likely to be transported directly if they had lower Glasgow Comma Scale scores, had penetrating injuries, were involved in traffic-related injuries, were closer to a Level IV or I trauma center, and if an advanced life support emergency medical service agency transported them from the scene. Patients were more likely to initially stop if they required advanced airway management, met at least one anatomic criterion, were further away from a Level I trauma center, or closer to an intermediate facility. CONCLUSIONS:: Confounding due to unadjusted prehospital factors may be present in studies evaluating the impact of directness of transport on short-term mortality outcomes. Propensity score analysis of treatment indications provides an additional and efficient method to reduce this bias. Language: en

Autoantibodies to ribosomal P (ribo P) are found in 15-30% of systemic lupus erythematosus (SLE) patients and are highly specific for SLE. The goal of this study is to assess the temporal association of anti-ribosomal P (anti-P) responses with SLE disease onset, as well as to characterize select humoral ribo P epitopes targeted in early, pre-diagnostic SLE samples. Patients with stored serial serum samples available prior to SLE diagnosis were identified from a military cohort. Each sample was tested for antibodies against ribo P utilizing standard C terminus ribo P enzyme-linked immunosorbent assays (ELISA) and a solid phase, bead-based assay with affinity-purified ribo P proteins. In this study, antibodies to ribo P were more common in African American SLE patients (p = 0.026), and anti-P-positive patients comprised a group with more measured autoantibody specificities than did other SLE patients (3.5 vs 2.2, p < 0.05). Antibodies against ribo P were present on average 1.7 years before SLE diagnosis and were detected an average of 1.08 years earlier in pre-diagnostic SLE samples using affinity-purified whole protein rather than C-terminal peptide alone (p = 0.0019). Furthermore, 61% of anti-P-positive patients initially had antibodies to aa 99-113, a known ribosomal P0 antigenic target, at a time point when no antibodies to the clinically used C terminus were detected. Our findings provide evidence that antibodies against ribosomal P frequently develop before clinical SLE diagnosis and are more broadly reactive than previously thought by targeting regions outside of the C terminus.

This study of tobacco exposure and auditory processes was conducted in a predominantly low-income population of 40 pregnant women and their newborns. Urinary cotinine concentrations and self-reported smoking status were obtained from the mother during the first prenatal care visit. Auditory brainstem-evoked responses (ABRs) were recorded in neonates to assess neuroelectrical activity of the auditory nerve following a sound stimulus. Infants of mothers with the highest cotinine concentrations (1,000 ng/ml) responded at a rate that was four times greater (hazard ratio 4.1, 95% confidence interval 1.4-11.5) than infants of non-smoking mothers (cotinineor= 15 ng/ml). Associations with more moderate cotinine concentrations (15-1,000 ng/ml) were not observed. Enhanced ABRs may disrupt auditory processes related to speech perception, negatively affecting reading and language development during childhood. The results suggest that tobacco exposure during pregnancy may impair auditory function.

Reports of the incidence of ITP are few and their methodology is variable. Accurate estimates of the incidence of immune thrombocytopenic purpura (ITP) are important to understand the medical and public health impact of the disease. To critically review all published reports on the incidence of ITP in children and adults, all articles identified on the Medline database (searched January 1, 1966-August 7, 2009) that reported data on the incidence of ITP were retrieved. Articles which directly estimated the incidence of ITP were selected for review. Eight articles reported the incidence of acute ITP in children. After review, four were determined to have the strongest estimates, based on the method of patient identification and study design. The lowest incidence estimate in these four studies was 2.2 per 10(5) children/year (95% confidence interval 1.9, 2.4) and the highest incidence estimate was 5.3 per 10(5) children/year (95% confidence interval 4.3, 6.4). Three studies reported the incidence of ITP in adults. The estimate from the article with the strongest methodology reported an incidence estimate of 3.3 per 10(5) adults/year. The current strongest estimate of the incidence of acute ITP in children is between 1.9 and 6.4 per 10(5) children/year; for adults the current strongest estimate of the incidence of ITP is 3.3 per 10(5) adults/year. An important limitation of these studies is that they are primarily from Europe and may not be generalizable to all regions.

Objective. To evaluate the extent to which seemingly healthy, mature adults with mild symptoms of dry eyes or dry mouth share the immunologic features found in patients with Sjogren's syndrome. Methods. Of 705 subjects in Malmo, Sweden (age range 52–72 years) who responded to a questionnaire, 35% reported some symptoms of dry eyes or mouth. A random subgroup of the symptomatic subjects (n = 77) and an age- and sex-matched control group from among the asymptomatic subjects (n = 32) were evaluated objectively by serologic testing and by various measures of exocrine gland function. Results. The symptomatic subjects had relatively impaired exocrine gland function and elevated levels of anti-Ro and anti-La (1.54–2.88-fold increase compared with the asymptomatic subjects, 95% confidence interval [CI] 1.41, 4.03). The 2 autoantibodies correlated with each other (r = 0.64, 95% CI 0.49, 0.78) as well as with selected clinical measures of glandular function. Conclusion. The association between self-reported symptoms of dry eyes or dry mouth and anti-Ro and anti-La, found in more than one-third of mature adults in this study, suggests that the immune abnormalities and exocrine gland dysfunction found in Sjogren's syndrome affect a substantial proportion of the general population.

To evaluate the economic effect of a pharmacy benefit expansion on a population of Oklahoma Medicaid recipients and to determine whether recipients who routinely maximized their monthly prescription limit (cap) before the benefit expansion benefited more from the expansion than the remainder of the study population.Retrospective study.Oklahoma Medicaid claims data from January 1, 2003, to December 31, 2004.Data from 15,936 Oklahoma Medicaid recipients.Retrospective administrative analysis using the Oklahoma Health Care Authority pharmacy and medical claims databases.Total health care expenditures per recipient per year, total medical expenditures per recipient per year, and total pharmacy expenditures per recipient per year.Total health care expenditures increased 17% after the benefit expansion (P0.0001). Of this increase, 65% was attributed to pharmacy expenditures and 35% to medical expenditures. However, a subpopulation of recipients who routinely reached their prescription limit before the expansion had a statistically significant increase in total and pharmacy expenditures; a statistically significant increase in medical expenditures was not observed.Although total health care expenditures increased after a monthly pharmacy benefit in a Medicaid population was expanded, a subpopulation of recipients identified as high pharmacy users before the expansion did not have a statistically significant increase in medical expenditures, whereas those who were non-high users experienced a significant increase. Additionally, this subpopulation experienced a nonsignificant decrease in hospital expenditures. These results could suggest that this subpopulation was affected differently than the overall population by the expansion of the Medicaid pharmacy benefit.

Type I IFNs are potent regulators of innate and adaptive immunity and are implicated in the pathogenesis of systemic lupus erythematosus. Here we report that clinical and pathological lupus nephritis and serum anti-nuclear Ab levels are greatly attenuated in New Zealand Mixed (NZM) 2328 mice deficient in type I IFN receptors (IFNAR). To determine whether the inflammatory environment in NZM 2328 mice leads to IFNAR-regulated changes in dendritic cells (DC), the number, activation, and function of DC subsets were compared in 2- and 5-mo-old (clinically healthy) female NZM and NZM-IFNAR−/− mice. Numbers of activated CD40high plasmacytoid DC (pDC) were significantly increased in renal lymph nodes of 2-mo-old NZM but not NZM-IFNAR−/− mice, suggesting an early IFNAR-dependent expansion and activation of pDC at disease sites. Relative to NZM spleens, NZM-IFNAR−/− spleens in 5-mo-old mice were significantly decreased in size and contained reduced numbers of conventional DC subsets, but not pDC. Splenic and renal lymph node NZM-IFNAR−/− DC analyzed directly ex vivo expressed significantly less CD40, CD86, and PDL1 than did NZM DC. Upon activation with synthetic TLR9 ligands in vitro, splenic NZM-IFNAR−/− DC produced less IL-12p40/70 and TNF-α than did NZM DC. The limited IFNAR−/− DC response to endogenous activating stimuli correlated with reduced numbers of splenic activated memory CD4+ T cells and CD19+ B cells in older mice. Thus, IFNAR signaling significantly increases DC numbers, acquisition of Ag presentation competence, and proinflammatory function before onset of clinically apparent lupus disease.

Purpose: To determine adherence to the American Academy of Pediatrics guidelines for thyroid screening in children with Down syndrome among primary care providers in the states of Oklahoma and Nebraska. Methods: We sought to identify all children with Down syndrome born in Oklahoma and Nebraska between 1994 and 2004 and review their medical records for evidence of thyroid screening. Patients were identified through a State Department of Health birth defects registry in Oklahoma and through participation in genetics clinics and laboratories in Nebraska and Oklahoma. Charts obtained from primary care providers were reviewed and the number of actual thyroid screens was compared with the number of recommended screens for each individual during the study period. Results: In Oklahoma, 13% of participating children received all thyroid screens recommended in the guidelines. In Nebraska, 14% of children received all recommended thyroid screenings. Among participants in Oklahoma, a mean of 34% of recommended thyroid screenings were performed. In Nebraska, a mean of 45% of recommended thyroid screenings were performed. Conclusions: The level of adherence to the American Academy of Pediatrics guidelines for thyroid screening in children with Down syndrome is low. Factors contributing to this low level of adherence need to be identified and addressed.

Objectives.—The aims of this study were to determine and compare fetal hemoglobin (HbF) fractions at birth in newborns exposed and not exposed to selected factors that have been reported to increase the risk of sudden infant death syndrome (SIDS). Previous studies have implicated HbF in the etiology of SIDS by finding higher fractions in infants dying from SIDS compared to age-matched control infants.Design.—We performed a cross-sectional study using high-performance liquid chromatography to measure HbF fractions in newborn cord blood samples. Exposure to selected risk factors for SIDS was assessed through review of medical records.Participants.—Six hundred thirty-three infants born at Via Christi Regional Medical Center–St Francis Campus, Wichita, Kan, from February 28 through August 5, 1997.Main Outcome Measure.—Hemoglobin F fractions at birth were compared in newborns exposed and not exposed to selected risk factors associated with increased incidence of SIDS.Results.—Mean HbF fractions were significantly higher in preterm newborns of mothers who smoked and in term newborns with intrauterine growth restriction, pregnancy weight gain less than or equal to 9 kg, and pregnancy complications associated with reduced placental blood flow. An elevated newborn HbF fraction, defined as 77% or greater, was significantly associated with maternal smoking, maternal anemia, intrauterine growth restriction, and pregnancy complications associated with reduced placental blood flow.Conclusion.—This study suggests a possible mechanism (HbF) by which previously identified factors may increase the risk of SIDS.

Purpose: This study describes the personal and practice characteristics of oral and maxillofacial surgeons, with an emphasis on gender differences. Potential explanations for differences found are offered. Materials and Methods: A 39-item questionnaire was designed to address areas of suspected differences between male and female oral and maxillofacial surgeons. It included items regarding training, certification, practice type and location, time spent working, practice composition, and personal characteristics. Identical questionnaires were sent to all of the 130 female oral and maxillofacial surgeons (OMSs) registered with AAOMS, as well as to 264 randomly sampled male OMSs. Results: Of the 192 responses received, 109 were from male surgeons, and 83 were from females, 56.8% versus 43.2% of the total. For men, the response rate was 41.3%, whereas the rate was 68.3% for the women; overall, 48.7% of the 394 oral surgeons responded. Profiles of the “average” male and female OMS showed similarities with regard to race, training, and reasons for choosing an OMS career. Age, marital status, number of children, physical characteristics, and use of time outside of work indicated some significant personal differences, as did practice characteristics, including income, number of years in practice, hours spent working, and number of patients seen. Clear gender-based trends were found regarding opinions of physical and mechanical disadvantages, with women more strongly denying such problems. A variety of both positive and negative viewpoints were elicited by the free comment section. Conclusions: Although male and female OMSs are similar with regard to most variables investigated, some significant differences do exist.

SUMMARYSystemic lupus erythematosus is associated with the presence of autoantibodies which bind several ribonucleoproteins, including Ro (or SS-A). We have explored the relationship of the HLA-DQ and T cell receptor alleles in patients producing autoantibodies binding the 13-kD carboxyl terminus fragment of the 60-kD Ro and with autoantibodies binding a peptide epitope within this fragment (amino acid residues 480 494). Antibodies binding the 13-kD fragment are more likely to be found in the sera of patients with particular DQA1 and DQB1 alleles, while antibodies binding the epitope at 480–494 are found almost exclusively in the sera of patients with a Bg/II 9–8-kb polymorphism of the T cell receptor β gene. Meanwhile, in these same patient sera the level of autoantibodies binding the complete 60-kD Ro particle is associated with a distinct pattern of alleles at these same immunoregulatory loci. These data demonstrate that component parts of autoantibody responses may be under genetic control which can be distinguished from the HLA associations characteristic of the response to the intact, complete autoantigen.

There is powerful evidence suggesting that etiology and pathogenesis of systemic lupus erythematosus has both genetic and environmental components. Unfortunately, understanding the genetics of lupus has been impeded by knowing the pattern of inheritance. Indeed, a complex mode of inheritance for the lupus disease phenotype is suggested by the known characteristics of this disorder. Twenty-five multiplex pedigrees for lupus have been enrolled and have been used to evaluate power to reveal linkage. The power to find linkage in these pedigrees is greater for autosomal recessive than for autosomal dominant modes of inheritance. Once 100 similar pedigrees are available for analysis our results predict that linkage is likely to be present for genetic models with relatively relaxed requirements. At loci operating by autosomal recessive inheritance linkage should be detectable despite genetic homogeneity as low as 40% and penetrance as low as 50%. For loci operating by autosomal dominant inheritance genetic homogeneity must be 60% or more when penetrance is as low as 50% to be able to establish linkage. Available preliminary data are also consistent with a possible genetic linkage of FCgammaRIIIpmn with lupus in American Black pedigrees multiplex for lupus. J Invest Dermatol 103:144S-149S, 1994

Clinicians have often noted that aberrant root morphology in a given tooth is also observed with varying degrees of frequency in the corresponding contralateral tooth. The purpose of this study was to determine the proportion of bilateral morphological root aberrations in a random sample of adult human dentition. Five hundred one dental records were selected from the retired record section at the University of Oklahoma College of Dentistry and their full-mouth radiographs were reviewed for aberrant root canal morphology. Bifurcation of the canal in mandibular first premolars was the most common finding (22.8% of patients), with 60% of these being bilateral. Maxillary anterior teeth had the least aberrations. It was observed that unusual root morphology is bilateral approximately 60% of the time. Therefore, the incidence of root or root canal abnormalities reported by the percentage of patients involved will always exceed the incidence of abnormalities reported by type of tooth (e.g. mandibular or canine) involved except for abnormalities which are found bilaterally in 100% of the patients studied. Radiographic interpretation appears to result in a lower incidence of anatomical aberrations than direct identification. The more rare the aberration, the more likely it is to be bilateral in occurrence.

Objective. To determine the presence of antibodies that bind vesicular stomatitis virus (VSV) proteins in systemic lupus erythematosus (SLE) patient sera, as well as to examine any relationship between antibodies binding the viral nucleocapsid (N) protein and anti-Ro autoantibodies. Methods. Eighty SLE patient sera, 80 normal control sera, 47 rheumatic disease patient control sera, and 9 sera from Panamanian subjects (6 of whom were infected with VSV) were evaluated by immunoblot of purified VSV proteins. Results. Findings on immunoblots of the Panamanian subjects' sera were consistent with histories of endemic exposure to VSV, as determined by virus neutralization assays. Significantly different binding to viral proteins was seen in the group of 80 SLE patients compared with the normal control group and with the rheumatic disease control group, by a variety of measures. For example, most of the reactivity in the SLE patient sera included binding to the internal viral matrix (M) and N proteins, while the reactivity in the normal control sera was mostly against the surface viral glycoprotein (G) protein alone or the N protein alone. Within this SLE patient cohort, associations were found between binding to N protein and anti-Ro precipitins and between binding to M protein and anti–nuclear RNP autoantibody precipitins. Conclusion. The data are consistent with the original specific hypotheses of a relationship between 60-kd Ro autoantigenicity and VSV, as well as with the suggestion that a rhabdovirus may be important in SLE. They do not, however, make possible any conclusions concerning the role of rhabdoviruses in the development of SLE or of anti-Ro autoimmunity.

Summary The RNA encoded by the 3′untranslated region of the prohibitin gene arrests cell proliferation by blocking the transition between the G1 and S phases of the cell cycle. The product of a variant allele (T allele) is inactive. We did a casecontrol study of prohibitin genotype in 205 women with breast cancer and 1046 healthy controls. The results showed an association between the T allele and breast cancer in women who reported a first-degree relative with the disease (odds ratio 2·5, p=0·005). An even stronger association was found in a subset of women diagnosed at or before age 50 years (4·8, p=0·003). These data suggest that prohibitin genotyping has value in assessing risk of breast cancer in women aged 50 years or younger with at least one first-degree relative with the disease.

Introduction : Knowing the prevalence of ITP is important to determine the burden of this rare disease. Multiple new thrombopoietin agonists are being developed for the treatment of ITP, despite the paucity of reliable and generalizable estimates of ITP prevalence. Only two studies have previously reported the prevalence of ITP in the United States (US) (the only other prevalence estimate focused on children with chronic ITP in the United Kingdom). Segal et al (J Thromb Haemost2006; 4:2377–2383) report a one-year age adjusted prevalence of 9.5 per 100,000 persons aged 1–64 years; Feudjo-Tepie et al (J Thromb Haemost2008; 6:711–712) report a one-year prevalence of adult chronic ITP of 23.6 per 100,000 adults 318 years of age. Both studies based their estimates on private insurance claims data. The goal of this study was to determine the prevalence of ITP in all patients in the State of Oklahoma, regardless of insurance status and age. Methods : Similar to the previous 2 studies, the ICD-9-CM code of 287.3 was used to identify ITP. Unlike the previous 2 studies, we obtained data directly and entirely from hematologists. In November 2007, there were 93 hematologists in Oklahoma who cared for ITP patients. Our preliminary data documented that hematologists saw 3 92% of all patients with ITP and that primary care physicians in Oklahoma reported they were ‘likely’ to refer 85% of patients with platelet counts 16 years), and the overall population. The denominator was the Oklahoma population (US Census 2000). Results : The 2003 prevalence estimates were: 8.8 per 100,000 children, 11.6 per 100,000 adults, and 11.0 overall per 100,000 persons. The 2004 prevalence estimates were: 7.4 per 100,000 children, 12.6 per 100,000 adults, and 11.4 overall per 100,000 persons. The average annual prevalence estimates were: 8.1 per 100,000 children (95% CI 6.7, 9.5), 12.1 per 100,000 adults (95%CI 11.1, 13.0), and overall 11.2 per 100,000 persons (95% CI 10.4, 12.0). The children were 51% female, 49% male, and the average age was six years. Adults were 57% female, 43% male, and the average age was 55 years. Conclusion : This is the first population based study to determine the prevalence of ITP for an entire defined geographic region, regardless of insurance status and age. These results represent the most generalizable estimates of prevalence currently available on which to determine the burden of ITP. Results from this study should be generalizable because the demographics of Oklahoma closely resemble the demographics of the US. Additionally, these results confirm and extend the previously published prevalence estimate of Segal et al, 2006. This information is important not only for pharmaceutical companies, regulatory agencies, and heath care authorities, but also for patients with ITP.

A strong gene interaction between HLA-DQ1 and DQ2 alleles has been associated with anti-Ro/SSA autoantibodies (Harley, J.B., M. Reichlin, F. C. Arnett, E. L. Alexander, W. B. Bias, and T. T. Provost. 1986. Science [Wash. DC]. 232:1145-1147; Harley, J. B., A. S. Sestak, L. G. Willis, S. M. Fu, J. A. Hansen, and M. Reichlin. 1989. Arthritis Rheum. 32:826-836; Hamilton, R. G., J. B. Harley, W. B. Bias, M. Roebber, M. Reichlin, M. C. Hochberg, and F. C. Arnett. 1988. Arthritis Rheum. 31:496-505). To test a gene complementation mechanism for these results, restriction fragment length polymorphisms (RFLP) of the DQ alpha and DQ beta genes have been related to Ro/SSA precipitins in patients with systemic lupus erythematosus. In this study Ro/SSA precipitins are related to the simultaneous presence of a particular pair of RFLPs. A DQ alpha RFLP associated with HLA-DQ1 and a DQ beta RFLP associated with HLA-DQ2 predict that the alpha beta heterodimer in HLA-DQ1/DQ2 heteroxygotes is most closely related to anti-Ro/SSA autoantibodies, thereby supporting a gene complementation mechanism. Beyond this effect, an RFLP associated with HLA-DQ2 and/or DR7 is also related to Ro/SSA precipitins. Multiple molecular histocompatibility mechanisms are implicated, therefore, in the production of anti-Ro/SSA autoantibodies in autoimmune disease. For anti-Ro/SSA autoantibodies in SLE, and perhaps more generally, these data show that the histocompatibility antigens are among the elements that confer autoimmune response specificity and restrict the production of particular autoantibodies among patients with systemic lupus erythematosus.