Rural and urban disparities in caries prevalence in children with unmet dental needs: the New England Children's Amalgam Trial

OBJECTIVES: To compare the prevalence of caries between rural and urban children with unmet dental health needs who participated in the New England Children's Amalgam Trial. METHODS: Baseline tooth and surface caries were clinically assessed in children from rural Maine (n = 243) and urban Boston (n = 291), who were aged 6 to 10 years, with two or more posterior carious teeth and no previous amalgam restorations. Statistical analyses used negative binomial models for primary dentition caries and zero-inflated models for permanent dentition caries. RESULTS: Urban children had a higher mean number of carious primary surfaces (8.5 versus 7.4) and teeth (4.5 versus 3.9) than rural children. The difference remained statistically significant after adjusting for sociodemographic factors and toothbrushing frequency. In permanent dentition, urban children were approximately three times as likely to have any carious surfaces or teeth. However, rural/urban dwelling was not statistically significant in the linear analysis of caries prevalence among children with any permanent dentition caries. Covariates that were statistically significant in all models were age and number of teeth. Toothbrushing frequency was also important for permanent teeth. Conclusions: Within this population of New England children with unmet oral health needs, significant differences were apparent between rural and urban children in the extent of untreated dental decay. Results indicate that families who agree to participate in programs offering reduced cost or free dental care may present with varying amounts of dental need based on geographic location.     

Dietary macronutrients, cholesterol, and sodium and lower urinary tract symptoms in men

Background

Little is known about dietary correlates of lower urinary tract symptoms (LUTS).

Objective

To examine associations between dietary intakes of total energy, carbohydrates, protein, fats, cholesterol, and sodium and LUTS in men.

Design, setting, and participants

Cross-sectional study of 1545 men aged 30–79 yr in the Boston Area Community Health survey (2002–2005), a random population-based sample. Dietary data were assessed by validated self-administered food frequency questionnaire. LUTS and covariate data were collected during in-person interviews. Primary analyses used multivariate logistic regression.

Measurements

Outcomes were moderate to severe LUTS, storage symptoms, and voiding symptoms as measured by the American Urological Association Symptom Index.

Results and limitations

Greater total energy intake was associated with higher LUTS symptom score (p_trend < 0.01) and increased likelihood of storage symptoms. No associations were observed with total, saturated, or monounsaturated fat intake or carbohydrates. Men who consumed more protein were less likely to report LUTS, particularly voiding symptoms (quintile 5 vs quintile 1 OR = 0.35; 95% CI, 0.17–0.74; p = 0.006). Sodium intake had positive linear associations with LUTS (p_trend = 0.01) and storage symptom score (p_trend = 0.004); this finding should be confirmed by studies using biomarkers of sodium exposure. Storage symptoms increased slightly with greater polyunsaturated fat intake (p_trend = 0.006). Data on specific polyunsaturated fats were unavailable.

Conclusions

This community-based study of men found that total energy and sodium intake were positively associated with LUTS, whereas greater protein intake was inversely associated with LUTS.     

Pharmacokinetic parameters of nevirapine and efavirenz in relation to antiretroviral efficacy

Optimal adherence is essential for successful antiretroviral therapy. We analyzed the relation between minimum plasma drug concentration (Cmin) and total drug exposure over 24 hr (AUC24) with virologic failure for therapy-adherent patients in the nevirapine (NVP) and efavirenz (EFV) groups of the double nonnucleoside study (2NN), which compared the efficacy of NVP and/or EFV together with stavudine and lamivudine. The objective was to find cutoff values of the Cmin and AUC24 below which the risk of virologic failure increased. The relation between Cmin and AUC24 with virologic failure (never a plasma viral load [pVL] < 50 copies/ml or a rebound to two consecutive pVL > 50 copies/ml) was analyzed with proportional hazard analyses. Data were censored at end of study or change of allocated treatment. The risk of virologic failure with NVP (n = 511) started to increase at a Cmin < 3.1 mg/L (hazard ratio [HR], 1.33; 95% confidence interval [CI], 0.89-1.97), but there was no cutoff value below which a statistically significant increased risk occurred. Neither was such a cutoff point identified for the AUC24. The risk of virologic failure with EFV (n = 312) was significantly increased at a Cmin < 1.1 mg/L (HR, 1.95; 95% CI, 1.08-3.54) and an AUC24 < 40 mg x hr x L1 (HR, 1.95; 95% CI, 1.07-3.54). Both cutoff values represent the median values for adherent patients. These associations were driven by patients from Thailand. Adjusting for geographical region made the association between Cmin and AUC24 with virologic failure statistically nonsignificant. The sensitivity of the Cmin values was too low (29% for NVP, 64% for EFV) to be an adequate predictor for virologic failure. We conclude that identifying the Cmin value for the sole purpose of predicting virologic failure in patients who report to be adherent to NVP or EFV is questionable because of the absence of a concentration-response relation (NVP) or the low sensitivity for such a cutoff value (NVP and EFV).     

Synergistic effects of butyrate on platelet responses to arachidonate, A23187, PGE1, and forskolin

With eukaryotic cells, butyrate is known to induce a series of morphological and biochemical changes that mimic cellular differentiation. With platelets, we have found that butyrate (10 mmol/L) caused an approximately threefold increase in sensitivity to calcium ionophore A23187 and arachidonate. Maximum aggregation was observed at agonist concentrations of 3 mumol/L and 170 mumol/L, respectively, as compared with required concentrations of 10 mumol/L and 400 mumol/L in the absence of butyrate. Similar effects were seen with isobutyric acid, and about one-half the effect was shown with valerate and caproate, but lower homologues showed no synergistic effect. No ultrastructural changes were observed in platelets incubated with butyrate, and the aggregation effects were reversible and returned to normal on removal of butyrate. Membrane fluidity was unchanged by butyrate as measured by changes in the fluorescence depolarization of diphenylhexatriene. Butyrate caused a 60% to 70% increase in the uptake of 3H-arachidonate. Butyrate also potentiated the inhibition of platelet function by prostaglandin E1 and forskolin and uptake of 3H- forskolin was increased approximately 20%. In contrast, platelet response to other agonists (ADP, epinephrine, collagen, thrombin, and platelet-activating factor) was essentially unaffected by butyrate. These results suggest that butyrate may increase the uptake of certain hydophobic agonists and antagonists by platelets. Similar mechanisms for uptake of endogenous effectors may explain the response of eukaryotic cells to butyrate in culture.     

Oral administration of the growth hormone secretagogue NN703 in adult patients with growth hormone deficiency

OBJECTIVE: Little is known of the usefulness of GH secretagogues (GHSs) in GH-deficient (GHD) adults. The objective of this study was to determine the number of responders to treatment with NN703 in GHD adults. DESIGN: A multicentre, randomized, double-blind, and placebo-controlled study. PATIENTS: Ninety-seven GHD adults were included. MEASUREMENTS: The GH response before and after 1 week of oral treatment with NN703 (n = 83) or placebo (n = 14) was determined. The first and last dose of NN703 was 3 mg/kg, whereas the dose of NN703 was 1.5 mg/kg/day during the 6 days between the first and last doses. Furthermore, all 97 patients received 1 micro g/kg GH-releasing hormone (GHRH) 3 weeks after the last dose of NN703. RESULTS: Serum GH peak and area under curve (AUC) values after the first NN703 administration were greater than those after placebo administration (P < 0.05). However, after correction for the lower body mass index (BMI) in the NN703 group, this difference lost statistical significance. After 1 week of therapy, GH peak and AUC values were similar following the final doses of NN703 and placebo. Serum peak and AUC values of other anterior pituitary hormones were similar between the NN703 and placebo groups both after the first and last administration of study drug. Nine of the 83 patients (11%) responded with a serum peak GH concentration >or= 5 micro g/l after the first and/or last NN703 administration, whereas no patient responded after placebo administration. Serum IGF-I was unaffected by 1-week NN703 treatment, whereas serum IGFBP-3 was increased (P < 0.05 vs. placebo) also after correction for BMI. Mean serum peak GH concentration after GHRH administration was 2.1 micro g/l (+/-0.3, SEM), which was higher than that after the first NN703 administration (1.32 +/- 0.3, P < 0.05). CONCLUSION: NN703 administration was generally well tolerated. Eleven per cent of the GHD adult patients responded with a peak GH response >or= 5 micro g/l after the first and/or last administration of oral NN703. Although a majority of GHD adults will not respond to NN703, the present results suggest that oral NN703 treatment could be useful in some adult patients with moderately severe GHD. These patients may be identified by a test dose of GHS.     

Do Physicians Attend to Base Rates? Prevalence Data and Statistical Discrimination in the Diagnosis of Coronary Heart Disease

Objective. To examine whether physicians attend to gender prevalence data in diagnostic decision making for coronary heart disease (CHD) and to test the hypothesis that previously reported gender differences in CHD diagnostic certainty are due to discrimination arising from reliance on prevalence data (“statistical discrimination”). Data Sources. A vignette‐based experiment of 256 randomly sampled primary care physicians conducted from 2006 to 2007. Study Design. Factorial experiment. Physicians observed patient presentations of cardinal CHD symptoms, standardized across design factors (gender, race, age, socioeconomic status). Data Collection. Structured interview. Principal Findings. Most physicians perceived the U.S. population CHD prevalence as higher in men (48.4 percent) or similar by gender (44.9 percent). For the observed patient, 52 percent did not change their CHD diagnostic certainty based on patient gender. Forty‐eight percent of physicians were inconsistent in their population‐level and individual‐level CHD assessments. Physicians' assessments of CHD prevalence did not attenuate the observed gender effect in diagnostic certainty for the individual patient. Conclusions. Given an adequate presentation of CHD symptoms, physicians may deviate from their prevalence data during diagnostic decision making. Physicians' priors on CHD prevalence did not explain the gender effect in CHD certainty. Future research should examine personal stereotypes as an explanation for gender differences.