A novel dispensing system based on two coaxial needles is used to fabricate three dimensional, periodic scaffolds by rapid prototyping.

Objectives. Fibroblast growth factor-23 (FGF-23) and vitamin D are hormones involved in phosphate homoeostasis. They also directly influence cardiomyocyte hypertrophy. We examined whether the relationships between levels of vitamin D or FGF-23, cardiac phenotype and outcome were independent of established cardiac biomarkers in a large cohort of community-dwelling elderly subjects.Design and Setting. Plasma levels of FGF-23 and vitamin D were measured in 1851 men and women (65-84 years) resident in the Lazio region of Italy. Participants were referred to eight cardiology centres for clinical examination, electrocardiography, comprehensive Doppler echocardiography and blood sampling. All-cause mortality or hospitalizations were available after a median follow-up of 47 months with record linkage of administrative data.Results. Vitamin D deficiency (<20 ng mL Conclusions. In community-dwelling elderly individuals with highly prevalent vitamin D deficiency, FGF-23 levels were associated with LV hypertrophy and predicted mortality independently of two robust cardiac biomarkers. A causal relationship was not demonstrated, but the hormones involved in mineral metabolism emerged as nontraditional risk factors and may affect cardiovascular risk.

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Summary dose of 5.5 mg/kg of T IV followed by maintenance IV doses ofThe metabolic pathway of theophylline (T) was studied in 12 newborns, one young infant, six children, and three adult volunteers. T was injected IV, and blood and urine samples were assayed for T, caffeine (C), and their metabolites by a high-pressure liquid chromatography technique. We confirmed the methylation of T to C in newborn infants but not in older subjects. Demethylation of T to Imethylxanthine was found in the young infant, in children, and in adults, but not in newborns. The major products excreted by neonates were T, 1-methyluric acid, and 1.3-dimethyluric acid. Children excreted a larger fraction of methyluric acids than adults.Renal and body clearance of T and C are reported and discussed in relation to the age. SpeculationOn the grounds of blood and urine samples from subjects treated with theovvlline. our results could indicate that caffeine oxidation over N-demethylation, involving lower activity of the cytochrome P-450 monooxygenase system during the first month of life than in older infants or adults compared to data reported in literature for other drugs. Our results suggest different forms of enzymes are involved in these reactions.Since its introduction in the treatment of apnea the disposition of theophylline (T) has been well described, not only in children (18)(19)(20)32) and adults (10, 11,13,15,16,22,26,29,30,31), but also in the premature neonate. Newborns eliminate the drug very slowly (4,12,17,23,28) partially methylating it to caffeine (C) (7-9). a unique example of drug methylation in humans.T is metabolized in the liver by the P-450-dependent microsomal system, which has been shown to be deficient in the newborn, in relation to several substrates (25).Methylxanthine metabolism has been studied in the adult (5. l I, 15, 29-3 1 ) but except for the paper by Aldridge et al. (I ) on caffeine no data have been published so far on children and neonates. This study was undertaken to: (1) further study the unusual metabolism of T to C; (2) define the metabolic pattern of T in neonates; (3) describe progressive changes of T metabolism during development.

Background Studies assessing whether heart failure (HF) is associated with an excess risk of cancer and cancer-related mortality yielded conflicting results. Here, we assessed the incidence and mortality of cancer according to the presence of HF in a community-based cohort. Methods By reviewing the health care records of the Puglia region in Italy, we first selected individuals ≥50-year-old, with no history of cancer within 3 years before the baseline evaluation and ≥5 years of follow-up, during the period from January 1st, 2005 to December 31st, 2013. Next, we matched 1:1 104,020 subjects with HF at baseline and 104,020 controls based on age, sex, Charlson Comorbidity Index, Drug-Derived Complexity Index, and follow-up duration. Cancer incidence and mortality were analyzed by Kaplan-Meier method and Cox regression models. Fine and Grey's regression model was also used to compare cancer-specific mortality while taking into account the competing risk of non-cancer death. Results Overall, the mean age of the study population was 76±10 years and the mean follow-up was 5.7 years. The incidence rate of cancer in HF patients and controls was 21.36 (95% CI, 20.98–21.74) and 12.42 (95% CI, 12.14–12.72) per 1000 person/years, respectively, corresponding to a 76% higher risk of incident cancer in HF patients (HR, 1.76; 95% CI, 1.71–1.81). HF patients also died from cancer more frequently than controls (HR 4.11; 95% CI, 3.86–4.38; Figure 1). This excess mortality was highest when age was &lt;70 years (HR 7.54, 95% CI 6.33–8.98), and declined in subjects aged 70–79 years (HR 3.80, 95% CI 3.44–4.19) and ≥80 years (HR 3.10, 95% CI 2.81–3.43). The association of HF with cancer mortality was confirmed in the competing risk analysis (HR 3.48, 95% CI 3.27–3.72), as well as the interaction with age: &lt;70 years of age: HR 6.65, 95% CI 5.60–7.94; 70–80 years: HR 3.14, 95% CI 2.84–3.48; and ≥80 years: HR 2.81, 95% CI 2.55–3.10. The HF-related risk applied to the majority of cancer types, with the exception of neoplasm of the male reproductive system. Interestingly, among HF patients a high consumption of loop diuretic (&gt;37.5 mg/d of furosemide) was associated with a higher mortality for cancer (HR 1.34, 95% CI 1.26–1.42 vs. ≤37.5 mg/d). Conclusions The analysis of this large community-based sample suggests that HF does portend an increased risk of cancer and cancer-related mortality, which is blunted, yet remains substantial, with increasing age and competing risk of dying from other causes. The risk of cancer may be heightened when HF is poorly compensated. Funding Acknowledgement Type of funding sources: None. Figure 1. Cancer mortality in HF patient