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Aim To investigate, with extended follow-up, cause-specific mortality among low-income Black and White Americans with Type 2 diabetes who have similar socio-economic status. Methods Black and White Americans aged 40–79 years with Type 2 diabetes (n = 12 498) were recruited from community health centres as part of the Southern Community Cohort Study. Multivariable Cox analysis was used to estimate mortality hazard ratios and 95% CIs for subsequent cause-specific mortality, based on both underlying and contributing causes of death. Results During the follow-up (median 5.9 years), 13.3% of the study population died. The leading causes of death in each race were ischaemic heart disease, respiratory disorders, cancer, renal failure and heart failure; however, Blacks were at a lower risk of dying from ischaemic heart disease (hazard ratio 0.70, 95% CI 0.54–0.91) or respiratory disorders (hazard ratio 0.70, 0.53–0.92) than Whites but had higher or similar mortality attributable to renal failure (hazard ratio 1.57, 95% CI 1.02–2.40), heart failure (hazard ratio 1.47, 95% CI 0.98–2.19) and cancer (hazard ratio 0.87, 95% CI 0.62–1.22). Risk factors for each cause of death were generally similar in each race. Conclusions These findings suggest that the leading causes of death and their risk factors are largely similar among Black and White Americans with diabetes. For the two leading causes of death in each race, however, ischaemic heart disease and respiratory disorders, the magnitude of risk is lower among Black Americans and contributes to their higher survival rates.

OBJECTIVE To determine if long-term mortality rates in early-onset insulin-treated diabetes differ by race among adults of similar socioeconomic status. RESEARCH DESIGN AND METHODS A total of 391 (299 African Americans, 92 whites) mostly low-income adults 40–79 years of age with insulin-treated diabetes diagnosed before 30 years of age were recruited from community health centers in the southeast U.S. Cox models were used to estimate hazard ratios (HRs) of all-cause mortality among African Americans compared with whites. Additionally, standardized mortality ratios (SMRs) were used to compare the mortality experience of the individuals with diabetes with both national and general community health center sex- and race-specific population norms. RESULTS Mean age at diabetes diagnosis and cohort entry, respectively, was 21 and 50 years in African Americans and 19 and 51 years in whites. During an average of 6.7 years of follow-up, 29% of African Americans and 35% of whites died. In multivariable analysis, no significant mortality difference was observed among African Americans compared with whites (HR 0.83 [95% CI 0.53–1.30]; P = 0.51). Compared with the race-specific U.S. general population, SMRs for those with diabetes were 5.7 in African Americans and 11.7 in whites. However, when compared with the same source population (i.e., the community health center population), SMRs were 3.5 and 3.7 in African Americans and whites, respectively. CONCLUSIONS Elevated mortality persists in men and women with long duration of early-onset insulin-treated diabetes, but given survival to 40 years of age and similarly low economic status and access to health care, our data do not suggest a racial disparity in mortality.

Law enforcement agencies stress that public reporting of terror-related crime is the predominant means for disrupting these actions. However, schools may be unprepared because the majority of the populace may not understand the threat of suspicious materials or what to do when they are found on school grounds. The purpose of this study was to systematically teach preschool children to identify and report suspicious packages across three experiments. In the first experiment, we used multiple exemplar training to teach children to identify the characteristics of safe and unsafe packages. In the second experiment, we taught participants to identify the locations where packages should be considered unsafe. Finally, in the third experiment, we used behavioral skills training to teach participants to avoid touching unsafe packages, leave the area where they were located, and report their discovery to an adult. Results suggest the participants quickly developed these skills. Implications for safety skills in young school children are discussed.

Advances in gene–environment interaction research have revealed genes that are associated with aggression. However, little is known about parent perceptions of genetic screening for behavioral symptoms like aggression as opposed to diagnosing disabilities. These perceptions may influence future research endeavors involving genetic linkage studies to behavior, including proactive approaches for parents to avoid events leading to aggression. The purpose of this study was to solicit the perspectives of parents who have children with autism about screening for genes associated with aggression, compared to responses from those who have children without disabilities and those planning to have children. Parents of children with autism were more likely to support screening and the use of the results to seek treatment if necessary. Results are discussed in the context of surveillance screening and systematic early intervention for behavioral symptoms related to autism. The results may provide insight for clincians, researchers, policymakers, and advocacy groups related to diagnosing and treating aggression in people with autism.

OBJECTIVE To estimate mortality rates and risk factors for mortality in a low-socioeconomic status (SES) population of African Americans and whites with diabetes. RESEARCH DESIGN AND METHODS We determined mortality among African Americans and whites aged 40–79 years with (n = 12,498) and without (n = 49,914) diabetes at entry into a cohort of participants recruited from government-funded community health centers. Multivariable Cox analysis was used to estimate mortality hazard ratios (HRs) (95% CI) among those with versus those without diabetes and among those with diabetes according to patient characteristics. RESULTS During follow-up (mean 5.9 years), 13.5% of those with and 7.3% of those without diabetes died. All-cause mortality risk was higher among those with versus without diabetes for both African Americans (HR 1.84 [95% CI 1.71–1.99]) and whites (1.80 [1.58–2.04]), although among those with diabetes, mortality was lower among African Americans than whites (0.78 [0.69–0.87]). Mortality risk increased with duration of diabetes and was greater among patients on insulin therapy and reporting histories of cardiovascular disease (CVD), hypertension, and stroke. The HRs associated with these multiple risk factors tended to be similar by sex and race, with the exception of a differentially higher impact of prevalent CVD on mortality among African Americans (interaction P value = 0.03), despite a lower baseline prevalence of CVD. CONCLUSIONS In this population with similarly low SES and access to health care, strong and generally similar predictors of mortality were identified for African Americans and whites with diabetes, with African Americans at a moderately but significantly lower mortality risk.

OBJECTIVE In young-onset diabetes, insulin therapy status is a rough marker of diabetes type. We describe the mortality experience of a low-income, predominantly minority population with diabetes diagnosed before age 30 years, stratified by insulin therapy. RESEARCH DESIGN AND METHODS A total of 1,098 adults aged 40–79 years (median 49) diagnosed with diabetes before age 30 years and 49,914 without diabetes were recruited from community health centers. Individuals with diabetes were categorized by insulin therapy at baseline: group A, insulin therapy only; group B, insulin therapy and an oral hypoglycemic agent; and group C, no insulin therapy. Cox models were used to compute hazard ratios (HRs) and 95% CI for cause-specific mortality based on both underlying and contributing causes of death from death certificates. RESULTS During follow-up (mean 3.9 years), 15.0, 12.5, and 7.3% of groups A, B, and C, respectively, and 4.6% without diabetes died. Compared with individuals without diabetes, HRs (CI) for all-cause mortality were 4.3 (3.4–5.6), 4.2 (2.8–6.3), and 2.0 (1.4–2.8) in groups A, B, and C, respectively. The leading cause of death was renal failure (end-stage renal disease [ESRD]) in group A, ESRD and coronary artery disease (CAD) in group B, and CAD in group C and individuals without diabetes. HRs for these conditions were at least twice as high as the HRs for all-cause mortality, reaching 17.3 (10.2–29.3), 17.9 (8.3–38.7), and 5.1 (2.3–11.7) in groups A, B, and C, respectively, for ESRD. CONCLUSIONS Excess mortality persists among people with young-onset diabetes of long duration, with ESRD and CAD as the leading contributors to mortality.

Research on aggression over the past two decades has focused on gene–environment interaction models to explain the relative contribution of each to this behavioral phenotype in various clinical populations. Recent investigations suggest a link between aggression in people with intellectual disabilities the functionality of the serotonin transporter. The aims in this study were to examine the possible association of the STin2 and/or the 5-HTTLPR serotonin transporter polymorphisms in adult males with and without intellectual disabilities, and to examine the association of these polymorphisms with aggression in people with intellectual disabilities. DNA samples and behavioral records were obtained from adult males with intellectual disabilities, distinguished only by the presence or absence of aggression. No association was found between either transporter polymorphism for aggression. However, the long 5-HTTLPR allele, and not the short allele or the heterozygous state, was associated with the severity of aggression. The association with aggression appears to be genetically complex, suggesting there may be other genes, interactions between genes, and/or environmental relations occasioning aggression in people with intellectual disabilities.

A functional polymorphism in the promoter of the gene encoding monoamine oxidase A has been associated with problem behavior in various populations. We examined the association of MAOA alleles in adult males with intellectual/developmental disabilities with and without established histories of problem behavior. These data were compared with a gender, ethnicity, and age-matched contrast sample. About 43% (15/35) of adults with intellectual/developmental disabilities and problem behavior possessed the low-efficiency version of the MAOA gene. In comparison, 20% (7/35) of adults with intellectual/developmental disabilities and no problem behavior and 20% (7/35) of the contrast group had the short-allele MAOA polymorphism. Therefore, a common variant in the MAOA gene may be associated with problem behavior in adults with intellectual/developmental disabilities.

Objective Hyperglycemia worsens clinical outcomes in critically ill patients. Precise glycemia control using intravenous insulin improves outcomes. To determine if we could improve glycemia control over a previous paper-based, manual protocol, authors implemented, in a surgical intensive care unit (SICU), an intravenous insulin protocol integrated into a care provider order entry (CPOE) system. Design Retrospective before-after study of consecutive adult patients admitted to a SICU during pre (manual protocol, 32 days) and post (computer-based protocol, 49 days) periods. Measurements Percentage of glucose readings in ideal range of 70–109 mg/dl, and minutes spent in ideal range of control during the first 5 days of SICU stay. Results The computer-based protocol reduced time from first glucose measurement to initiation of insulin protocol, improved the percentage of all SICU glucose readings in the ideal range, and improved control in patients on IV insulin for ≥24 hours. Hypoglycemia ( Conclusion The CPOE-based intravenous insulin protocol improved glycemia control in SICU patients compared to a previous manual protocol, and reduced time to insulin therapy initiation. Integrating a computer-based insulin protocol into a CPOE system achieved efficient, safe, and effective glycemia control in SICU patients.

Elderly patients with diabetes are at increased fracture risk. Although long exposure to hyperglycemia may increase fracture risk via adverse effects on bone metabolism, tight glycemic control may increase risk via trauma subsequent to hypoglycemia. We tested the prospective relationship between glycemic control and fracture risk in 10,572 elderly patients (age ≥65) with diabetes.Geriatric patients with diabetes were drawn from Vanderbilt University Medical Center's Electronic Health Record. Baseline was defined as age at first HbA1c after the latter of age 65 or ICD 9 code for diabetes. Cox analysis was used to test the relationship of updated mean HbA1c (average HbA1c over follow-up) with time to first fracture since baseline. HbA1c was categorized as follows:6.5% [48mmol/mol]; 6.5-6.9% [48-52mmol/mol]; 7-7.9% [53-63mmol/mol]; 8-8.9% [64-74 mmol-mol]; ≥9% [≥75mmol/mol]. The number of BMI measurements was used as a surrogate for relative frequency of outpatient visits, i.e. patient-provider contacts.During follow-up, there were 949 fracture events. HbA1c demonstrated a cubic relationship with fracture risk (p0.05). In analyses accounting for age, sex, race, and number of BMI measures (a surrogate for patient-provider interaction), compared to an HbA1c of 7-7.9%, HRs (95% CIs) were: HbA1c6.5% HR=0.97 (0.82-1.14), 6.5-6.9% HR=0.80 (0.66-0.97), 8-8.9% HR=1.13 (0.92-1.40), ≥9% HR=1.19 (0.93-1.54).An HbA1c of 6.5-6.9% is associated with the lowest risk of fracture in elderly patients with diabetes. Risk associated with an HbA1c ≥9% may be a marker of infrequent patient-provider interaction.

Purpose Radiation oncology (RO) residency applicants commonly use Internet resources for information on residency programs. The purpose of this study is to assess the accessibility, availability, and quality of online information for RO graduate medical education. Methods and materials Accessibility of online information was determined by surveying databases for RO residency programs within the Fellowship Residency Electronic Interactive Data Access System (FREIDA) of the American Medical Association, the Accreditation Council for Graduate Medical Education (ACGME), and Google search. As of June 30, 2015, websites were assessed for presence, accessibility, and overall content availability based on a 55-item list of desired features based on 13 program features important to previously surveyed applicants. Quality scoring of available content was performed based on previously published Likert scale variables deemed desirable to RO applicants. Quality score labels were given based on percentage of desired information presented. Results FREIDA and ACGME databases listed 89% and 98% of program websites, respectively, but only 56% and 52% of links routed to a RO department-specific website, respectively. Google search obtained websites for 98% of programs and 95% of links routed to RO department-specific websites. The majority of websites had program descriptions (98%) and information on staff. However, resident information was more limited (total number [42%], education [47%], previous residents [28%], positions available [35%], contact information [13%]). Based on quality scoring, program websites contained only 47% of desired information on average. Only 13% of programs had superior websites containing 80% or more of desired information. Conclusions Compared with Google, the FREIDA and ACGME program databases provide limited access to RO residency websites. The overall information availability and quality of information within RO residency websites varies widely. Applicants and programs may benefit from improved content accessibility and quality from US RO program websites in the residency application process.

From an applied behavior-analytic perspective, aggression in people with intellectual disabilities is mostly maintained by social reinforcement consequences. However, nonsocial consequences have also been identified in functional assessments on aggression. Behaviors producing their own reinforcement have been labeled "automatic" or "nonsocial" in the behavior-analytic literature, a label that bares a striking resemblance to biobehavioral explanations of reward-seeking behaviors. Biobehavioral studies have revealed that aggression activates the same endogenous brain mechanisms as primary reinforcers like food. Therefore, integrating brain-environment explanations would result in a better understanding of the functional mechanisms associated with nonsocial aggression. The purpose of this paper was to explore aggression as a reinforcing consequence for reinforcement-seeking behaviors in people with intellectual disabilities. First, the literature establishing aggression as reinforcement for arbitrary responding will be reviewed. Next, the reward-related biological process associated with aggression was described. Finally, the paper discusses what might be done to assess and treat aggression maintained by nonsocial reinforcement.

Two experiments were conducted to test the effect of a room with sensory equipment, or Snoezelen room, on the stereotypic behavior and engagement of adults with profound mental retardation. In Experiment 1, participants were observed in their living room before and after attending the Snoezelen room. Results showed that there tended to be a reduction in stereotypy and increase in engagement when participants went from their living room to the Snoezelen room, and a return of these behaviors to pre-Snoezelen levels in the living room. Positive effects in the Snoezelen room did not carryover to the living room. In Experiment 2, the living and Snoezelen rooms were compared to an outdoor activity condition with the same participants and target behaviors. Results showed that the outdoor condition was superior, the Snoezelen condition intermediate, and the living room least effective in their impact on stereotypic behavior and engagement. Conceptualizations regarding factors that maintain stereotypic behavior and engagement were discussed in the context of the three experimental conditions.

The effects of hypercalcemia on the heart and the resulting alterations of the electrocardiogram are well established. However, there are only rare reports of arrhythmias caused by hypercalcemia in primary hyperparathyroidism. This article describes a case of severe hypercalcemia secondary to hyperparathyroidism causing tachy-brady syndrome.

Variation in the distribution of dietary nitrogen among the different amino acids is one factor that can modify the calorie equivalent per weight of amino acid or protein. This is important to consider when experimental diets with different amino acid compositions are compared and when indirect calorimetry is used to determine substrate oxidation rates. We developed a computer program to compute the energy content, oxygen equivalent, and respiratory quotient for arbitrary mixtures of amino acids and representative carbohydrates and fats. The calorie content of individual free amino acids was calculated by correction of the heat of combustion for the incomplete oxidation of amino acids characteristic of humans. Although these computations were presented before, we not report the limit of applicability of published values and the availability of the computer program to do these calculations.

Patients with acute exacerbation of chronic obstructive pulmonary disease (COPD) frequently report a history of theophylline use prior to arrival in the emergency department. The reliability of using this history to guide aminophylline therapy is, however, unclear. The authors studied patients with an acute exacerbation of COPD to determine the relation between the initial theophylline level and the medication history. Seventy-nine patients with a mean age of 64.3 years were entered into the study. The average theophylline level was 10.8 micrograms/mL. Forty-seven percent of the patients had subtherapeutic levels, 46% had therapeutic levels, and 7% had toxic levels. There were weak although statistically significant correlations between the theophylline level and the interval since the last theophylline dose (r = -.40, P less than .001), as well as with the last recorded outpatient theophylline level (r = .45, P less than .001). However, the theophylline level could not be predicted accurately in a number of patients. The authors conclude, because the prediction rule was often inaccurate, aminophylline therapy in patients with acute exacerbation of COPD should be based on direct measurement of the serum theophylline level.

Retrospective analysis of the rapid adrenocorticotropic hormone (ACTH) test in a large adult population shows a marked interdependence of the basal cortisol concentration, peak cortisol concentration, and increase in cortisol concentration. Repetition of the rapid ACTH test in the same patient does not improve diagnostic accuracy. A significant number of falsely abnormal rapid ACTH test results were observed (in comparison to continuous ACTH infusion as a reference test). This supports the use of the rapid ACTH test as a screening test, but not as a diagnostic test for adrenocortical failure. It is proposed that a peak cortisol level greater than or equal to 20 micrograms/dl (550 nmol/liter) is a sufficient single criterion for normal adrenal function as assessed by the rapid ACTH test.

Previous studies have established spirometric criteria for arterial blood gas analysis during acute asthmatic attacks. However, only general guidelines have been available regarding the need for blood gas analysis during an acute exacerbation of chronic obstructive pulmonary disease (COPD). We conducted a study to determine the relationship between arterial blood gases and spirometry in 70 emergency department patients during acute exacerbations of COPD. Arterial blood gas analysis and spirometry were performed on arrival at the emergency department. All of the patients with a pCO2 of more than 45 mm Hg had an FEV1 of less than 35% of the predicted normal. We found patients with a pO2 of less than 60 mm Hg who had an FEV1 as high as 54% of the predicted normal. There was no correlation between the FEV1 and pO2. Because spirometry was not reliable for identifying patients with significant hypoxemia, we conclude that arterial blood gas analysis is indicated for patients presenting to the ED with acute exacerbations of COPD. Spirometric criteria that have been used to eliminate the need for arterial blood gases in asthmatic patients cannot be applied safely to patients with COPD.

Thyrotoxicosis from an overdose of medicinal thyroid is a condition which may be associated with a significant delay in onset of toxicity. We report a case treated with plasmapheresis, and conclude that the amount of thyroid hormone removed was insignificant compared to the total ingestion. We also note that the plasma half-life of thyroxine is apparently reduced in an acute massive ingestion.

Amino acid availability rapidly regulates protein synthesis and degradation. Increasing amino acid concentrations above the levels found in post-absorptive plasma stimulates protein synthesis in a dose-dependent manner at the level of mRNA translation-initiation and inhibits protein degradation by inhibiting lysosomal autophagy. The anabolic effects of insulin on protein synthesis and protein degradation are exerted at the same sites (i.e., peptide chain initiation and lysosomal stabilization) allowing for a rapid synergistic response when both amino acids and insulin increase after a protein-containing meal. In perfused liver preparations, protein anabolic effects are exerted by a group of amino acids acting in concert. The BCAA are among the amino acids required for stimulation of hepatic protein synthesis, but there is no evidence that BCAA or leucine alone are effective. Leucine alone is an important inhibitor of hepatic protein degradation, but maximal inhibition requires in addition several other regulatory amino acids. In heart and skeletal muscle in vitro, increasing the concentration of the three BCAA or of leucine alone reproduces the effects of increasing the supply of all amino acids in stimulating protein synthesis and inhibiting protein degradation. Skeletal muscle is the largest repository of metabolically active protein and a major contributor to total body nitrogen balance. Supplying energy alone (i.e., carbohydrate and lipids) cannot prevent negative nitrogen balance (net protein catabolism) in animals or humans; only provision of amino acids allows the attainment of nitrogen balance. In rats and in humans nourished parenterally, provision of balanced amino acid solutions or of only the three BCAA cause similar improvements in nitrogen balance for several days. There is some evidence that infusions of leucine alone can stimulate muscle protein synthesis in vivo; the effect may be transitory and was not observed by all investigators; provisions of excess leucine alone does not seem to affect total body or muscle protein degradation in vivo. In postabsorptive rats, in vivo, infusion of the three BCAA together stimulates muscle protein synthesis as much as the infusion of a complete amino acid mixture or of a mixture of essential amino acids; the in vivo effect requires coinfusion of glucose or of small (physiological) doses of insulin, suggesting synergism between insulin and amino acids.(ABSTRACT TRUNCATED AT 400 WORDS)

The quantitative effect of plasmapheresis on concentrations of intravascular solutes is described by a minimal two-compartment model, which allows exit to and entry from a nonplasma body pool of the solute. This novel method is simple and capable of determining endogenous metabolic turnover of physiologically important plasma constituents in both therapeutic and experimental settings. The model was suggested by the therapeutic use of plasmapheresis in hyperlipidemia, and the turnover rates of triglyceride and cholesterol were calculated for one patient treated with chronic plasmapheresis. It is concluded that at least a two-compartment model is necessary to quantitatively describe the effect of plasmapheresis on any substance that undergoes appreciable endogenous turnover (metabolic clearance rate greater than 1.1 times plasmapheresis rate when both rates are in units of volume per time). Calculation of endogenous turnover rate with the use of measurements of the concentration of a solute in plasma before and after plasmapheresis and in the total plasmapheresate and measurement of the volume of plasma removed, volume of plasma substitute infused, and total plasmapheresis time is detailed. This method avoids the use of isotopic labeling experiments. In turn, the endogenous turnover rate may predict the efficacy of therapeutic plasmapheresis.