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The article presents a study which analyzed the magniture and trends in gallbladder cancer (GBC) mortality in Chile as an indirect assessment of the potential impact of the Acceso Universal con Garantías Explécitas (AUGE) program on GBC mortality. Topics discussed include GBC mortality rates in women, age-specific mortality rates for GBC, and possible reasons for the decline in GBC mortality rate prior to initiation of the AUGE program.

Kisspeptin regulates reproduction via signaling through the receptor, Kiss1r, in GnRH neurons. However, both kisspeptin and Kiss1r are produced in several peripheral tissues, and recent studies have highlighted a role for kisspeptin signaling in metabolism and glucose homeostasis. We recently reported that Kiss1r knockout (KO) mice display a sexually dimorphic metabolic phenotype, with KO females displaying obesity, impaired metabolism, and glucose intolerance at 4-5 months of age. However, it remains unclear when this metabolic phenotype first emerges in development, or which aspects of the pleiotropic phenotype underlie the metabolic defects and which are secondary to the obesity. Here, we studied Kiss1r KO females at different ages, including several weeks before the emergence of body weight (BW) differences and later when obesity is present. We determined that at young adult ages (6 wk old), KO females already exhibit altered adiposity, leptin levels, metabolism, and energy expenditure, despite having normal BWs at this time. In contrast, food intake, water intake, and glucose tolerance are normal at young ages and only show impairments at older adult ages, suggesting that these impairments may be secondary to earlier alterations in metabolism and adiposity. We also demonstrate that, in addition to BW, all other facets of the adult metabolic phenotype persist even when gonadal sex steroids are similar between genotypes. Collectively, these data highlight the developmental emergence of a metabolic phenotype induced by disrupted kisspeptin signaling and reveal that multiple, but not all, aspects of this phenotype are already disrupted before detectable changes in BW.

Meningococcal disease has a case-fatality rate of 50% for patients not given treatment and 10%-20% for those given treatment (1,2). The causative agent is Neisseria meningitidis, for which 14 serogroups [...]

Background Chronic kidney disease (CKD) in children is characterized by severe growth failure. The growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis in uremic animals shows a post-receptor impaired phosphorylation of Janus kinase 2/signal transducer and activator of transcription (JAK-STAT) proteins. The objective of our study was to characterize the intracellular phosphorylation of JAK-STAT signaling in fibroblasts from children with CKD on chronic peritoneal dialysis (PD). Methods Serum GH-binding protein (GHBP), IGF-1 and IGFBP3 were measured in 15 prepubertal CKD stage-5 children on PD. Cytoplasmic JAK2, cytoplasmic/nuclear STAT5b and nuclear IGFBP3, acid-labile subunit (ALS) and IGF-1 mRNA expression were quantified in fibroblasts obtained from skin biopsies before and after stimulation with 200 ng/ml recombinant human growth hormone (rhGH). Phosphorylation activity at both the cytoplasmic and nuclear level was expressed as the ratio phosphorylated (p)/total (t) abundance of the product (p/t) at 30 and 60 min. Fifteen healthy children were recruited as the control group. Values were expressed in arbitrary units (AU) and normalized for comparison. Significance was defined as p < 0.05. Results Thirty minutes after rhGH stimulus, the cytoplasmic (p/t)JAK2 ratio was significantly lower in patients than in controls [median and interquartile range (IQR): 7.4 (4.56) vs. 20.5 (50.06) AU]. At 60 min after rhGH stimulation, median JAK2 phosphorylation activity was still significantly lower in the patients [7.14 (IQR 3.8) vs. 10.2 (IQR 29.8) AU; p < 0.05]. The increase in the cytoplasmic (p/t)STAT5b/[beta]-actin ratio was lower at both measurement points in the patients compared to the controls, without reaching statistical significance between groups. Median IGFBP3 mRNA abundance was significantly decreased in fibroblasts from uremic patients 24 h after rhGH stimulation compared to the healthy controls [1.27 (IQR 0.83) vs. 2.37 (IQR 0.80) AU]. Median ALS and IGF-1 mRNA expression changed in response to rhGH stimuli at 24 and 48 h. Conclusion In this study, children with CKD undergoing PD therapy showed an impaired phosphorylation of JAK2/STAT5b signaling in fibroblasts after GH stimulation, as well as impaired IGFBP3 mRNA abundance. Both impairments may be partially responsible for the observed resistance to the growth-promoting actions of GH in chronic kidney failure., Author(s): Francisca Ugarte[sup.1] , Carlos Irarrazabal[sup.1] , Jun Oh[sup.2] , Anne Dettmar[sup.2] , Maria L. Ceballos[sup.3] , Angelica Rojo[sup.3] , M. Jose Ibacache[sup.3] , Cristian Suazo[sup.1] , Mauricio Lozano[sup.1] , [...]

Background Cardiovascular disease (CVD) in patients on chronic peritoneal dialysis (PD) is a major cause of death and is closely linked to hypertension and volume overload. The mini-Pet has been proposed as a useful tool to evaluate free-water transport (FWT) and characterize ultra filtration across the peritoneum. Knowledge regarding FWT could be of great value to predict volume overload in PD patients. Our objective in this study was to characterize FWT through the peritoneum in children on PD. Methods We studied clinically stable patients with >2 months on PD. Exclusion criteria were a peritonitis episode up to 2 months prior to entrance into the study and active nephrotic syndrome. A 1-h mini-peritoneal equilibration test (mini-PET) was performed with 3.86% glucose. Calculations (see text for full definitions) were: Dip Na (Na dial [min.sub.60]-Na dial [min.sub.1]), Dip D/PNa (D/[PNa.sub.60]-D/[PNa.sub.1]), total Na removal (NaR = total Na [dial.sub.60] - Na [dial.sub.1]), ultra filtration small pores [(UFSP = [Na.sub.R] x 1,000)/[Na.sub.p]], and FWT (UF-UFSP). Peritoneal equilibration test (PET), left ventricular mass index (LVMI, g/[m.sup.2]), daily UF, and residual renal function were evaluated. Pearson's correlation coefficient was used to establish correlation between variables. Results Sixteen patients were included, with a mean age of 11.8 [+ or -] 3.8 years. Free water transport normalized to body surface area (BSA) ([FWT.sub.n]) was 133.9 ± 85.7 ml/[m.sup.2]; creatinine dialysate-to-plasma (D/P) and glucose dialysate at X dwell time-to-0 dwell time ([D.sub.x]/[D.sub.0]) ratios were 0.38 ± 0.1 and 0.65 ± 0.09, respectively. LVMI was 46.6 ± 14.8 g/[m.sup.2]; 2-h creatinine D/P and glucose [D.sub.x]/[D.sub.0] showed no correlation with [FWT.sub.n], UF, and LVMI. [FWT.sub.n] showed a significant inverse correlation with LVMI (r 0.58, p 0.02). Conclusions This study characterized FWT in PD children through the mini-PET. Left ventricular hypertrophy showed a high prevalence in this group, and a significant correlation between LVMI and FWT was found. FWT could be a useful tool to evaluate UF in PD children. Keywords Mini-PET * Adequacy * Peritoneal transport * Peritoneal dialysis * Free water transport * Peritoneal equilibrium test, Introduction Since the first description by Twardowski et al. almost 30 years ago, the peritoneal equilibrium test (PET) has been used to predict the optimal dialysis prescription [1]. Individuals who [...]

Special studies and isolated initiatives over the past several decades in low-, middle- and high-income countries have consistently shown inequalities in health among socioeconomic groups and by gender, race or ethnicity, geographical area and other measures associated with social advantage. Significant health inequalities linked to social (dis)advantage rather than to inherent biological differences are generally considered unfair or inequitable. Such health inequities are the main object of health development efforts, including global targets such as the Millennium Development Goals, which require monitoring to evaluate progress. However, most national health information systems (HIS) lack key information needed to assess and address health inequities, namely, reliable, longitudinal and representative data linking measures of health with measures of social status or advantage at the individual or small-area level. Without empirical documentation and monitoring of such inequities, as well as country-level capacity to use this information for effective planning and monitoring of progress in response to interventions, movement towards equity is unlikely to occur. This paper reviews core information requirements and potential databases and proposes short-term and longer term strategies for strengthening the capabilities of HIS for the analysis of health equity and discusses HIS-related entry points for supporting a culture of equity-oriented decision-making and policy development. Keywords Information systems/organization and administration/standards; Delivery of healthcare; Social justice; Health status indicators; Socioeconomic factors; Demography; Data collection; Databases, Factual; Policy making; Developing countries (source: MeSH, NLM). Mots cles Systeme information/organisation et administration/normes; Delivrance soins; Justice sociale; Indicateur etat sanitaire; Facteur socioeconomique; Demographie; Collecte donnees; Choix d&apos;une politique; Pays en developpement (source: MeSH, INSERM). Palabras clave Sistemas de informacion/organizacion y administracion/normas; Prestacion de atencion de salud; Justicia social; Indicadores de salud; Factores socioeconomicos; Demografia; Recoleccion de datos; Bases de datos factuales; Formulacion de politicas; Paises en desarrollo (fuente: DeCS, BIREME)., Introduction: why measure health equity? Health equity is the absence of health differences between more and less socially advantaged groups (1). Sen (2) and others have argued that health equity [...]