Long-term enlargement of the neo-aortic root and aortic arch following arch reconstruction in hypoplastic left heart syndrome.

BACKGROUND: Long-term enlargement of the aortic arch after aortic arch reconstruction in hypoplastic left heart syndrome is not well described. METHODS: Aortic arch measurements for 50 patients with hypoplastic left heart syndrome who achieved Fontan completion were converted to Pediatric Heart Network z-scores. Dimensions were assessed using linear mixed models, and differences among time points were evaluated with F-tests. Sub-analysis was conducted comparing Norwood (n = 36) with hybrid (n = 14) strategies. RESULTS: Median time to last imaging was 6.4 (interquartile range, 3.5-11.3) years. Before intervention, the main pulmonary artery was dilated, whereas the ascending aorta, transverse arch, and isthmus were hypoplastic. With aortic arch reconstruction, there were expected increases in all arch z-scores. The aortic arch continued to dilate after aortic arch reconstruction, reaching peak values at 7 months (neo-aortic complex: z = 6.9 [5.6-8.0]) or 12 months after stage I (ascending aorta: z = 6.1 [2.9-8.3]; transverse arch: z = 4.7 [3.0-5.9]). After peak values, there was a gradual decline in z-scores with most components still at least mildly dilated at 16 years (neo-aortic complex: z = 3.2 [3.1-3.9], ascending aorta: z = 3.9 [3.3-4.2]; transverse arch: z = 3.1 [2.5-3.7]) with abrupt caliber change at the isthmus: z = -0.8 (-1.1 to -0.3). Norwood and hybrid strategies showed similar enlargement profiles after 7 months of age. CONCLUSIONS: Neo-aortic root and aortic arch in hypoplastic left heart syndrome are enlarged early after aortic arch reconstruction and continue to enlarge out of proportion to normal controls until 12 months of age, with gradual decline in enlargement up to adolescence. Further work should focus on modifiable surgical factors that may prove important to optimize arch growth and geometry.

Global Emergency Medicine: A Review of the Literature From 2015.

OBJECTIVES: The Global Emergency Medicine Literature Review (GEMLR) conducts an annual search of peer-reviewed and gray literature relevant to global emergency medicine (EM) to identify, review, and disseminate the most important new research in this field to a global audience of academics and clinical practitioners. METHODS: This year 12,435 articles written in six languages were identified by our search. These articles were distributed among 20 reviewers for initial screening based on their relevance to the field of global EM. An additional two reviewers searched the gray literature. A total of 723 articles were deemed appropriate by at least one reviewer and approved by their editor for formal scoring of overall quality and importance. Two independent reviewers scored all articles. RESULTS: A total of 723 articles met our predetermined inclusion criteria and underwent full review. Sixty percent were categorized as emergency care in resource-limited settings (ECRLS), 17% as EM development (EMD), and 23% as disaster and humanitarian response (DHR). Twenty-four articles received scores of 18.5 or higher out of a maximum score 20 and were selected for formal summary and critique. Inter-rater reliability between reviewers gave an intraclass correlation coefficient of 0.71 (95% confidence interval = 0.66 to 0.75). Studies and reviews with a focus on infectious diseases, trauma, and the diagnosis and treatment of diseases common in resource-limited settings represented the majority of articles selected for final review. CONCLUSIONS: In 2015, there were almost twice as many articles found by our search compared to the 2014 review. The number of EMD articles increased, while the number ECRLS articles decreased. The number of DHR articles remained stable. As in prior years, the majority of articles focused on infectious diseases.

Effects of karanjin on cell cycle arrest and apoptosis in human A549, HepG2 and HL-60 cancer cells.

BACKGROUND: We have investigated the potential anticancer effects of karanjin, a principal furanoflavonol constituent of the Chinese medicine Fordia cauliflora, using cytotoxic assay, cell cycle arrest, and induction of apoptosis in three human cancer cell lines (A549, HepG2 and HL-60 cells). RESULTS: MTT cytotoxic assay showed that karanjin could inhibit the proliferation and viability of all three cancer cells. The induction of cell cycle arrest was observed via a PI (propidium iodide)/RNase Staining Buffer detection kit and analyzed by flow cytometry: karanjin could dose-dependently induce cell cycle arrest at G2/M phase in the three cell lines. Cell apoptosis was assessed by Annexin V-FITC/PI staining: all three cancer cells treated with karanjin exhibited significantly increased apoptotic rates, especially in the percentage of late apoptosis cells. CONCLUSION: Karanjin can induce cancer cell death through cell cycle arrest and enhance apoptosis. This compound may be effective clinically for cancer pharmacotherapy.

Effects of karanjin on cell cycle arrest and apoptosis in human A549, HepG2 and HL-60 cancer cells

BACKGROUND: We have investigated the potential anticancer effects of karanjin, a principal furanoflavonol constituent of the Chinese medicine Fordia cauliflora, using cytotoxic assay, cell cycle arrest, and induction of apoptosis in three human cancer cell lines (A549, HepG2 and HL-60 cells). RESULTS: MTT cytotoxic assay showed that karanjin could inhibit the proliferation and viability of all three cancer cells. The induction of cell cycle arrest was observed via a PI (propidium iodide)/RNase Staining Buffer detection kit and analyzed by flow cytometry: karanjin could dose-dependently induce cell cycle arrest at G2/M phase in the three cell lines. Cell apoptosis was assessed by Annexin V-FITC/PI staining: all three cancer cells treated with karanjin exhibited significantly increased apoptotic rates, especially in the percentage of late apoptosis cells. CONCLUSION: Karanjin can induce cancer cell death through cell cycle arrest and enhance apoptosis. This compound may be effective clinically for cancer pharmacotherapy.

Effects of passive smoking on snoring in preschool children.

OBJECTIVE: To examine the association between passive smoking and snoring in preschool children using parent-reported questionnaires and urine cotinine levels. STUDY DESIGN: This was a population-based cross-sectional survey of 2954 children aged 2-6 years in Hong Kong. Parent-reported questionnaires provided information on snoring and household smoking. One-third of children randomly chosen from the cohort provided urine samples for cotinine analysis. Increased urine cotinine was defined as urinary cotinine concentration ≥ 30 ng/mg creatinine. Using multivariate logistic regression analysis, we analyzed the association between snoring and passive smoking, controlling for potential confounders including age, sex, body mass index z-score, atopic diseases, recent upper respiratory tract infection, parental allergy, parental education, family income, and bedroom-sharing. RESULTS: A total of 2187 completed questionnaires were included in the final analysis, and 724 children provided urine samples for cotinine measurement. After adjustment for confounding factors, questionnaire-based household smoking (>10 cigarettes/d: OR = 2.22, 95% CI = 1.02-4.81) and increased urine cotinine (OR = 4.37, 95% CI = 1.13-16.95) were significant risk factors for habitual snoring (snoring ≥ 3 nights per week). For occasional snoring (snoring 1-2 nights per week), reported household smoking (1-10 cigarettes/d: OR = 1.41, 95% CI = 1.14-1.76; >10 cigarettes/d: OR = 1.56, 95% CI = 1.05-2.31), and increased urine cotinine (OR = 1.82, 95% CI = 1.03-3.20) were also identified as significant risk factors. A dose-effect relationship was found for snoring frequency and adjusted natural logarithms of urinary cotinine concentrations (P < .001). CONCLUSIONS: Environmental tobacco smoke exposure is an independent risk factor for snoring in preschool children. Parents' smoking cessation should be encouraged in management of childhood snoring.