Prevalence of the metabolic syndrome among children from six cities of China

<p>Abstract</p> <p>Background</p> <p>Metabolic syndrome (MetS) in childhood can increase the risk of cardiovascular disease, diabetes mellitus and dyslipidemia in adulthood, which is of increasing concern in transitional and advanced economies. The aim of the current study was to explore the prevalence of MetS among children from six cities of China.</p> <p>Methods</p> <p>A total of 8,764 children (4,495 boys, 4,269 girls) aged 7-11 years were randomly selected from 6 cities of China. MetS was mainly defined by the criteria proposed by International Diabetes Federation (IDF).</p> <p>Results</p> <p>The overall prevalence of MetS for children older than 10 years was 0.8% by IDF definition. Obese children had significantly higher MetS prevalence compared with their counterparts with overweight (6.6% vs. 0.9%, <it>p </it>< 0.01) and normal weight (6.6% vs. 0.05%, <it>p </it>< 0.01). The prevalence of abdominal obesity, high triglycerides, low high density lipoprotein cholesterol, hypertension and high glucose among obese children was 93.4%, 16.5%, 14.3%, 7.3% and 4.0%, respectively, which significantly higher than those among overweight children (37.0%, 6.1%, 10.0%, 4.2%, and 3.3%, respectively) and among normal weight children (1.2%, 3.3%, 4.0%, 1.7% and 2.5%, respectively). The proportion of children with at least one, two, and three items of the metabolic abnormalities were 25.0%, 5.4% and 0.9%, respectively. Metabolic abnormalities were also present in children under 10 years of age.</p> <p>Conclusions</p> <p>The early onset of MetS among children and relatively high proportions of children with at least one or two metabolic abnormalities in cities of China can increase the risk of developing MetS. It implies the necessity to take effective actions to control and prevent the rapid development of obesity among children in developing countries, especial those undergoing transition to a Western lifestyle.</p

Primaquine in vivax malaria: an update and review on management issues

Primaquine was officially licensed as an anti-malarial drug by the FDA in 1952. It has remained the only FDA licensed drug capable of clearing the intra-hepatic schizonts and hypnozoites of Plasmodium vivax. This update and review focuses on five major aspects of primaquine use in treatment of vivax malaria, namely: a) evidence of efficacy of primaquine for its current indications; b) potential hazards of its widespread use, c) critical analysis of reported resistance against primaquine containing regimens; d) evidence for combining primaquine with artemisinins in areas of chloroquine resistance; and e) the potential for replacement of primaquine with newer drugs

Interferon Regulatory Factor-1 (IRF-1) Shapes Both Innate and CD8+ T Cell Immune Responses against West Nile Virus Infection

Interferon regulatory factor (IRF)-1 is an immunomodulatory transcription factor that functions downstream of pathogen recognition receptor signaling and has been implicated as a regulator of type I interferon (IFN)-αβ expression and the immune response to virus infections. However, this role for IRF-1 remains controversial because altered type I IFN responses have not been systemically observed in IRF-1-/- mice. To evaluate the relationship of IRF-1 and immune regulation, we assessed West Nile virus (WNV) infectivity and the host response in IRF-1-/- cells and mice. IRF-1-/- mice were highly vulnerable to WNV infection with enhanced viral replication in peripheral tissues and rapid dissemination into the central nervous system. Ex vivo analysis revealed a cell-type specific antiviral role as IRF-1-/- macrophages supported enhanced WNV replication but infection was unaltered in IRF-1-/- fibroblasts. IRF-1 also had an independent and paradoxical effect on CD8+ T cell expansion. Although markedly fewer CD8+ T cells were observed in naïve animals as described previously, remarkably, IRF-1-/- mice rapidly expanded their pool of WNV-specific cytolytic CD8+ T cells. Adoptive transfer and in vitro proliferation experiments established both cell-intrinsic and cell-extrinsic effects of IRF-1 on the expansion of CD8+ T cells. Thus, IRF-1 restricts WNV infection by modulating the expression of innate antiviral effector molecules while shaping the antigen-specific CD8+ T cell response

Zebrafish con/disp1 reveals multiple spatiotemporal requirements for Hedgehog-signaling in craniofacial development

<p>Abstract</p> <p>Background</p> <p>The vertebrate head skeleton is derived largely from cranial neural crest cells (CNCC). Genetic studies in zebrafish and mice have established that the Hedgehog (Hh)-signaling pathway plays a critical role in craniofacial development, partly due to the pathway's role in CNCC development. Disruption of the Hh-signaling pathway in humans can lead to the spectral disorder of Holoprosencephaly (HPE), which is often characterized by a variety of craniofacial defects including midline facial clefting and cyclopia <abbrgrp><abbr bid="B1">1</abbr><abbr bid="B2">2</abbr></abbrgrp>. Previous work has uncovered a role for Hh-signaling in zebrafish dorsal neurocranium patterning and chondrogenesis, however Hh-signaling mutants have not been described with respect to the ventral pharyngeal arch (PA) skeleton. Lipid-modified Hh-ligands require the transmembrane-spanning receptor Dispatched 1 (Disp1) for proper secretion from Hh-synthesizing cells to the extracellular field where they act on target cells. Here we study <it>chameleon </it>mutants, lacking a functional <it>disp1</it>(<it>con/disp1</it>).</p> <p>Results</p> <p><it>con/disp1 </it>mutants display reduced and dysmorphic mandibular and hyoid arch cartilages and lack all ceratobranchial cartilage elements. CNCC specification and migration into the PA primorida occurs normally in <it>con/disp1 </it>mutants, however <it>disp1 </it>is necessary for post-migratory CNCC patterning and differentiation. We show that <it>disp1 </it>is required for post-migratory CNCC to become properly patterned within the first arch, while the gene is dispensable for CNCC condensation and patterning in more posterior arches. Upon residing in well-formed pharyngeal epithelium, neural crest condensations in the posterior PA fail to maintain expression of two transcription factors essential for chondrogenesis, <it>sox9a </it>and <it>dlx2a</it>, yet continue to robustly express other neural crest markers. Histology reveals that posterior arch residing-CNCC differentiate into fibrous-connective tissue, rather than becoming chondrocytes. Treatments with Cyclopamine, to inhibit Hh-signaling at different developmental stages, show that Hh-signaling is required during gastrulation for normal patterning of CNCC in the first PA, and then during the late pharyngula stage, to promote CNCC chondrogenesis within the posterior arches. Further, loss of <it>disp1 </it>disrupted normal expression of <it>bapx1 </it>and <it>gdf5</it>, markers of jaw joint patterning, thus resulting in jaw joint defects in <it>con/disp1 </it>mutant animals.</p> <p>Conclusion</p> <p>This study reveals novel requirements for Hh-signaling in the zebrafish PA skeleton and highlights the functional diversity and differential sensitivity of craniofacial tissues to Hh-signaling throughout the face, a finding that may help to explain the spectrum of human facial phenotypes characteristic of HPE.</p

Intertidal mangrove mudflat 240+239Pu signatures, confirming a 210Pb geochronology on the southeastern coast of Brazil

A sediment core was taken to determine if sediment accumulation rates could be conducted using 240+239Pu signatures in the coastal mangrove mudflats of southeastern Brazil. The results from this study show that 240+239Pu fallout activities are sufficient and well preserved in the coastal sediments of this region. Sediment accumulation rates determined from the 240+239Pu signatures were 4.4 mm/year and 4.1 from 210Pb (CIC) method. A sediment mixing coefficient rate was calculated using chlorophyll-a profile (9.5 cm2)