Similarities and Differences in the Epidemiology of Pyloric Stenosis and SIDS

Similar temporal declines in infantile hypertrophic pyloric stenosis (IHPS) and sudden infant death syndrome (SIDS) and other common features have led to hypotheses about a shared etiology. We carried out a population-based study to highlight similarities and differences between IHPS and SIDS. We used vital statistics and hospitalization data on all live births in Washington State, USA (1987–2009). Changes in IHPS and SIDS rates over time were quantified using rate ratios with 95 % confidence intervals (CI). The duration between birth and diagnosis of IHPS or SIDS was examined as a function of gestational age at birth. Logistic regression analysis was used to identify risk factors and quantify adjusted temporal trends (2000–2008). Although both IHPS and SIDS rates declined significantly between 1987 and 2008, the patterns and magnitude of the declines (40 and 74 %, respectively) were different. IHPS and SIDS shared risk factors such as maternal smoking and single parent status but other factors showed qualitatively or and quantitatively different associations. Primiparity was a risk factor for IHPS [odds ratio (OR) 1.24, 95 % CI 1.09–1.41], and a protective factor for SIDS (OR 0.44, 95 % CI 0.36–0.55), while male sex had a stronger association with IHPS (OR 4.51, 95 % CI 3.85–5.28 vs 1.36, 95 % CI 1.13–1.64). Both IHPS and SIDS showed significant inverse associations between gestational age at birth and chronologic age at diagnosis/death. IHPS and SIDS share some epidemiologic features and risk factors but other risk factors have qualitatively or quantitatively different effects and recent temporal trends in the two diseases are dissimilar.     

Phthalate metabolites in urine and asthma,allergic rhinoconjunctivitis and atopic dermatitis in preschool children

Phthalate esters are among the most ubiquitous of indoor pollutants and have been associated with various adverse health effects. In the present study we assessed the cross-sectional association between eight different phthalate metabolites in urine and allergic disease in young children. As part of the Danish Indoor Environment and Children's Health study, urine samples were collected from 440 children aged 3–5 years, of whom 222 were healthy controls, 68 were clinically diagnosed with asthma, 76 with rhinoconjunctivitis and 81 with atopic dermatitis (disease subgroups are not mutually exclusive; some children had more than one disease). There were no statistically significant differences in the urine concentrations of phthalate metabolites between cases and healthy controls with the exception of MnBP and MECPP, which were higher in healthy controls compared with the asthma case group. In the crude analysis MnBP and MiBP were negatively associated with asthma. In the analysis adjusted for multiple factors, only a weak positive association between MEP in urine and atopic dermatitis was found; there were no positive associations between any phthalate metabolites in urine and either asthma or rhinoconjunctivitis. These findings appear to contradict earlier studies. Differences may be due to higher exposures to certain phthalates (e.g., BBzP) via non-dietary pathways in earlier studies, phthalates serving as surrogates for an agent associated with asthma (e.g., PVC flooring) in previous studies but not the present study or altered cleaning habits and the use of “allergy friendly” products by parents of children with allergic disease in the current study in contrast to studies conducted earlier.     

Clinical and molecular characterisation of a prospectively collected cohort of children and adolescents with polycythemia vera

The clinical, haematological, molecular and treatment data of eight paediatric patients with polycythemia vera (PV) were collected prospectively. One patient developed PV after treatment for large-cell anaplastic lymphoma. Budd-Chiari syndrome was diagnosed in two patients, necessitating orthotopic liver transplantation in one and transjugular portosystemic shunting in the other. The remaining patients presented with non-specific symptoms. Endogenous erythroid colonies were detected in all cases examined. The JAK2 ^V617F mutation was found in six patients; two patients displayed JAK2 exon 12 mutations, including one novel mutation ( JAK2 ^{H538-K539delinsI}). CD177 ( PRV-1 ) mRNA expression was increased in three of five patients tested.     

Analysis of residual monomers in dendritic methacrylate copolymers and composites by HPLC and headspace-GC/MS.

OBJECTIVES: The aim of this study was to analyze the residual monomer content of photopolymerized dendritic methacrylate copolymers and particulate filler composites. Headspace-gas chromatography/mass spectrometry (HS-GC/MS) was compared with high performance liquid chromatography (HPLC). METHODS: The resin mixtures consisted of a dendritic methacrylate monomer, methyl methacrylate and acetoacetoxyethyl methacrylate in varied proportions. In addition, one of the composites contained 1,4-butanediol dimethacrylate. Camphorquinone and 2-(N,N-dimethylamino)ethyl methacrylate were used as the light-activated initiator system. The content of residual methyl methacrylate and acetoacetoxyethyl methacrylate after 40 s photopolymerization were analyzed with HPLC and HS-GC/MS. RESULTS: The content of residual methyl methacrylate decreased and residual acetoacetoxyethyl methacrylate increased with increasing concentration of acetoacetoxyethyl methacrylate in the resin mixture. The results with both methods had the same trend. SIGNIFICANCE: The addition of acetoacetoxyethyl methacrylate enhanced the copolymerization of methyl methacrylate, but did not decrease the total residual monomer content. The HS-GC/MS method was found to be a feasible method in the analysis of low-boiling residuals in dental polymers.     

Presence of heterozygous ATM deletion may not be critical in the primary response of chronic lymphocytic leukemia cells to fludarabine

Objectives: Abnormalities of the TP53 or ATM, cooperating tumor‐suppressor genes, significantly worsen the treatment options for chronic lymphocytic leukemia (CLL) patients. Although the aberrations seem to be mutually exclusive in this leukemia, inactivation of the former gene leads to worse prognosis. We tested the in vitro sensitivity of the CLL samples with heterozygous ATM deletion to fludarabine and combination of fludarabine and rituximab; the responses were compared with the TP53‐abnormal and wild‐type (wt) cells to delimitate relative significance of ATM deletion. Methods: In vitro analysis was performed on fifty‐nine characterized CLL samples using viability assay WST‐1. Western blot and real‐time RT‐PCR were used to monitor the activation of the ATM/p53 pathway. Results and conclusions: At the clinically relevant concentration of fludarabine, TP53‐abnormal samples exhibited markedly higher resistance to fludarabine than the remaining CLL samples (P = 0.012); cohort with ATM deletion was not more resistant than wt cells. A similar induction of the p53 protein and its downstream target genes PUMA and BAX in ATM‐deleted and wt cells confirmed that the former subgroup has preserved a critical pro‐apoptotic response. Proportions of the samples, which had been sensitized to fludarabine by rituximab pretreatment, were insignificantly lower (P = 0.22) in the TP53‐abnormal and ATM‐deleted subgroups compared to the wt cases (30%; 29%; 50%, respectively). The presence of ATM (11q22–23) deletion in the CLL cells should not be considered an indication of resistance to fludarabine or its combination with rituximab.