Overall Hospital Cost Estimates in Children with Congenital Heart Disease: Analysis of the 2012 Kid’s Inpatient Database

This study sought to determine overall hospital cost in children with congenital heart disease (CHD) and to compare cost associated with cardiac surgical procedures, cardiac catheterizations, non-cardiac surgical procedures, and medical admissions. The 2012 Healthcare Cost and Utilization Project Kid’s Inpatient Database was used to evaluate hospital cost in neonates and children with CHD undergoing cardiac surgery, cardiac catheterization, non-cardiac surgical procedures, and medical treatments. Multivariable logistic regression was applied to determine independent predictors for increased hospital cost. In 2012, total hospital cost was 28,900 M$, while hospital cost in children with CHD represented 23 % of this total and accounted for only 4.4 % of hospital discharges. The median cost was $51,302 ($32,088–$100,058) in children who underwent cardiac surgery, $21,920 ($13,068–$51,609) in children who underwent cardiac catheterization, $4134 ($1771–$10,253) in children who underwent non-cardiac surgery, and $23,062 ($5529–$71,887) in children admitted for medical treatments. Independent predictors for increased cost were hospital bed size <400 beds (P < 0.001), more than four procedures performed during the same hospitalization (P = 0.001), use of ECMO (P < 0.001), length of hospital stay exceeding 14 days (P < 0.001), cardiac failure (P < 0.001), sepsis (P < 0.001), acute kidney injury (P < 0.001), and neurologic (P < 0.001) and thromboembolic complications (P < 0.001). Hospital cost in children with CHD represented 23 % of global cost while accounting for only 4.4 % of discharges. This study identified factors associated with increased cost of cardiac surgical procedures, cardiac catheterizations, non-cardiac surgical procedures, and medical management in children with CHD.     

Dibucaine in Ionic-Gradient Liposomes: Biophysical,Toxicological, and Activity Characterization

Administration of local anesthetics is one of the most effective pain control techniques for postoperative analgesia. However, anesthetic agents easily diffuse into the injection site, limiting the time of anesthesia. One approach to prolong analgesia is to entrap local anesthetic agents in nanostructured carriers (e.g., liposomes). Here, we report that using an ammonium sulphate gradient was the best strategy to improve the encapsulation (62.6%) of dibucaine (DBC) into liposomes. Light scattering and nanotracking analyses were used to characterize vesicle properties, such as, size, polydispersity, zeta potentials, and number. In vitro kinetic experiments revealed the sustained release of DBC (50% in 7 h) from the liposomes. In addition, in vitro (3T3 cells in culture) and in vivo (zebrafish) toxicity assays revealed that ionic-gradient liposomes were able to reduce DBC cyto/cardiotoxicity and morphological changes in zebrafish larvae. Moreover, the anesthesia time attained after infiltrative administration in mice was longer with encapsulated DBC (27 h) than that with free DBC (11 h), at 320 μM (0.012%), confirming it as a promising long-acting liposome formulation for parenteral drug administration of DBC.     

Management of stress urinary incontinence with surface electromyography-assisted biofeedback in women of reproductive age

BACKGROUND AND PURPOSE: Although surgery has been widely accepted as the treatment of choice for stress urinary incontinence (SUI), there has recently been an increased interest in the conservative management of this condition. The aims of this study were to test the ability of a biofeedback-assisted pelvic-floor muscle exercise (PFME) program to affect symptoms of SUI in premenopausal women and to evaluate a training program that might lead to successful outcomes in a relatively limited number of sessions. SUBJECTS: Twenty-six women with SUI were treated with PFME with surface electromyography (sEMG)-assisted biofeedback. All participants were of reproductive age and were treated individually for 12 sessions. METHODS: results were evaluated with a 7-day voiding diary, a 1-hour pad test, pelvic-floor muscle strength measurements, sEMG amplitudes, a leakage index, and a quality-of-life questionnaire. These variables were compared before and after the intervention. RESULTS: The frequency of urine loss, the occurrence of nocturia, and the number of pads required decreased significantly after the intervention. Objective cure was found in 61.5% of women. There was a significant improvement in the quality of life, in pelvic-floor muscle strength, and in the sEMG amplitudes of all contractions throughout the intervention. DISCUSSION AND CONCLUSION: A relatively short-term intervention of PFME with sEMG-assisted biofeedback appeared to be helpful in relieving symptoms of SUI in premenopausal women and represents a reasonable conservative management option.     

Subtle improvement of seizure susceptibility by atorvastatin treatment during epileptogenesis

Background

The process by which a brain insult elicits epilepsy is termed epileptogenesis and it is characterized by numerous molecular and functional alterations. Statins are first-line drugs for hypercholesterolemia and related diseases, and display neuroprotective properties in clinical and experimental studies. Considering the importance in developing therapeutic strategies to prevent or modify epileptogenesis, we aimed the present study to test the hypothesis that atorvastatin modifies seizure susceptibility of mice after status epilepticus (SE).

Evidence for a limited role of NAD(P)H in the nutritional regulation of glucagon release: Studies with menadione and NH4Cl

Summary Menadione and NH₄Cl were reported to lower the islet content of reduced pyridine nucleotides. They were used to investigate the possible significance of NAD(P)H in the regulation of glucagon release by glucose and arginine. Menadione (10–25 μmol/l) enhanced arginine-stimulated glucagon release at a low glucose concentration (3.3 mmol/l), but failed both to affect glucagon secretion in the sole presence of glucose (3.3 mmol/l) and to suppress the inhibitory action of glucose 11.1 mmol/l upon glucagon output. In contrast to menadione, NH₄Cl inhibited arginine-stimulated glucagon release at the low glucose concentration. The inhibitory action of glucose in high concentration upon glucagon release was not suppressed by NH₄Cl. These findings do not permit to extrapolate to the A₂-cell the concept that reduced pyridine nucleotides represent a major coupling factor in the nutritional regulation of hormonal release.     

The multiple facets of the fat tissue

After a long history of relative neglect by the scientific community, white adipose tissue is finally emerging as a central component of body homeostasis. Indeed, the explosion of obesity statistics worldwide encouraged the study of adipose tissue and the complications of increased adiposity, such as insulin resistance, type 2 diabetes, and accelerated vascular disease. Far beyond merely furnishing free fatty acids from triglyceride depots, a growing list of fat tissue-derived mediators has increased the understanding of the regulatory role of adipose tissue in metabolic control. Recently, inflammation within the obese adipose tissue has surfaced as another important link of obesity to its undesirable metabolic consequences.