ABSTRACT: The most common approaches used today for the correction of sagittal synostosis involve large craniectomies and extensive cranial vault remodeling. Although these techniques ultimately yield very good cosmetic results, they have significant drawbacks. They are lengthy, expensive, associated with significant blood loss, universally require transfusions, and often result in prolonged hospitalization.We present here our 5-year experience with correction of sagittal synostosis using the recently described minimally invasive strip craniectomy followed by postoperative cranial vault helmet molding. During this period, we treated a total of 97 children with nonsyndromic single-suture synostosis. The first 46 of 67 children treated for sagittal synostosis had at least 1 year of postoperative follow-up and were included in the analysis. There were 33 boys and 13 girls. Patients' mean age at surgery was 3.1 months, and the mean weight was 6.1 kg. The mean operative time was 75 minutes. The estimated blood loss during the procedure was 56 mL. Eight patients received blood transfusions during surgery (17.4%) and 3 patients received after surgery (6.5%). There were no significant postoperative complications. The mean hospitalization was 2.2 days. Excellent aesthetic outcomes were noted in all patients. The change in cranial index from a preoperative value of 0.7 to 0.8 postoperatively was virtually stabilized 3 months after the surgical intervention. Significantly better correction rates were observed in the youngest patients.Because of its excellent attributes, minimally invasive strip craniectomy followed by postoperative helmet molding is likely to become the preferred treatment modality for the correction of sagittal synostosis.

BackgroundMandatory reporting of healthcare associated infections (HAI) is increasing. Evidence for agreement among different reviewers applying HAI surveillance criteria is limited. We aim to characterize agreement among Infection Preventionists (IPs) conducting surveillance for central line-associated bloodstream infection (CLABSI) with each other and as compared to simplified laboratory-based definitions.MethodsAbstracted electronic health records were assembled from in-patients with positive blood cultures at a tertiary care Veterans Affairs (VA) hospital over a 5-year period. Identical patient records were made available to VA IPs from different facilities to report on CLABSI using their usual surveillance methods. Positive blood cultures were also evaluated using laboratory-based definitions. Standard indices of inter-rater agreement, expressed as a kappa statistic, were computed between IPs, and between IPs and simplified laboratory-based methods.ResultsOverall, 114 patient records were reviewed by 18 IPs, the majority of whom specified they followed National Healthcare Safety Network (NHSN) criteria. The overall agreement amongst IPs by kappa was 0.42 (SE 0.06). IPs had better agreement with a simple laboratory-based definition with an average kappa of 0.55 (SE 0.05). The proportion of patient records that 18 IPs reported with CLABSI ranged from 14% to 39%(overall mean 28% with a CV of 25%). When simple laboratory-based methods were applied to different sets of patient records, classification was more consistent with CLABSI assigned in a proportion ranging from 36% to 42%(overall mean 39%).ConclusionReliability of IP-conducted surveillance to identify HAI may not be ideal for public reporting goals of inter-hospital comparisons.

BackgroundThe role of proximal tubule (PT) angiotensinogen (AGT) in modulating blood pressure has previously been examined using mice expressing PT human AGT and human renin, or rat AGT. These animals are hypertensive; however, the question remains whether alterations in mouse PT AGT alone affects arterial pressure.MethodsMouse AGT cDNA was knocked-in to the endogenous kidney androgen protein (KAP) gene using an internal ribosomal entry site (IRES)-based strategy.ResultsThe KAP-mAGT animals showed kidney-specific KAP-AGT mRNA expression; renal in situ hybridization detected KAP-AGT mRNA only in PT. Urinary AGT was markedly increased in KAP-mAGT mice. On a high Na diet, radiotelemetric arterial pressure showed a systolic pressure elevation; no significant difference in arterial pressure was observed on a normal diet. Plasma renin concentration (PRC) was reduced in KAP-mAGT animals given a high Na diet, but was not different between mouse lines during normal Na intake. Plasma AGT concentration was not altered by overexpression of PT mouse AGT.ConclusionsIn summary, PT overexpression of mouse AGT leads to salt-sensitive hypertension without recruitment of the systemic renin-angiotensin system.American Journal of Hypertension 2012; doi:10.1038/ajh.2012.16.

Background/Aims: To evaluate the efficacy and safety profile of S-1 combined with oxaliplatin (SOX) against unresectable advanced or metastatic gastric cancer. Methodology: Oxaliplatin was administered intravenously at 100mg/m2 for two hours on day 1 and S-1 was administered b.i.d. at 80mg/m2/day on days 1-14 followed by a 7-day rest during the 3-week schedule. Results: All 51 patients were assessed for efficacy and adverse events. The response and disease control rates were 41% and 90%, respectively. The response rate was significantly improved in patients with ECOG performance status of no more than 1, elevated CEA levels or unresected primary cancers. The median follow-up time was 11.8 months, the median time to progression was 6.8 months, the median overall survival was 11.8 months and the 1-year survival rate was 47.4%. Patients with diffused type exhibited significantly decreased time to progression and overall survival. The grade 3/4 adverse events were hematological toxicities, including neutropenia (13.7%), thrombocytopenia (13.7%) and anemia (11.8%). The incidence of grade 3/4 non-hematological events was low (≤2%). Conclusions: The SOX regimen (oxaliplatin, 100mg/m2 d1; S-1, 80mg/m2/day, b.i.d. d1-14, q3w) provided a favorable efficacy and safety profile in Chinese patients with advanced gastric cancer.

Flow coefficients v_{n} for n=2, 3, 4, characterizing the anisotropic collective flow in Au+Au collisions at sqrt[s_{NN}]=200  GeV, are measured relative to event planes Ψ_{n}, determined at large rapidity. We report v_{n} as a function of transverse momentum and collision centrality, and study the correlations among the event planes of different order n. The v_{n} are well described by hydrodynamic models which employ a Glauber Monte Carlo initial state geometry with fluctuations, providing additional constraining power on the interplay between initial conditions and the effects of viscosity as the system evolves. This new constraint can serve to improve the precision of the extracted shear viscosity to entropy density ratio η/s.

This study focused on the volatile organic compounds (VOCs) and metal leaching from three kinds of composite products made from fiberglass-resin portion (FRP) of crushed printed circuit board (PCB) waste, including phenolic molding compound (PMC), wood plastic composite (WPC), and nonmetallic plate (NMP). Released VOCs from the composite products were quantified by air sampling on adsorbent followed by thermal desorption and GC-MS analysis. The results showed that VOCs emitted from composite products originated from the added organic components during manufacturing process. Phenol in PMC panels came primarily from phenolic resin, and the airborne concentration of phenol emitted from PMC product was 59.4 ± 6.1 μg/m3, which was lower than odor threshold of 100% response for phenol (180 μg/m3). VOCs from WPC product mainly originated from wood flour, e.g. benzaldehyde, octanal, and d-limonene were emitted in relatively low concentrations. For VOCs emitted from NMP product, the airborne concentration of styrene was the highest (633 ± 67 μg/m3). Leaching characteristics of metal ions from composite products were tested using acetic acid buffer solution and sulphuric acid & nitric acid solution. Then the metal concentrations in the leachates were tested by ICP-AES. The results showed that only the concentration of Cu (average = 893 mg/L; limit = 100 mg/L) in the leachate solution of the FRP using acetic acid buffer solution exceeded the standard limit. However, other concentrations of metal ions (Pb, Cd, Cr, Ba and Ni) were within the standard limit. All the results indicated that the FRP in composite products was not a major concern in terms of environmental assessment based upon VOCs tests and leaching characteristics.

Genetic alterations of 16q21-q22, the locus of a 6-cadherin cluster, are frequently involved in multiple tumors, suggesting the presence of critical tumor suppressor genes (TSGs). Using 1 Mb array comparative genomic hybridization (aCGH), we refined a small hemizygous deletion (∼1 Mb) at 16q21-22.1, which contains a single gene Cadherin-11 (CDH11, OB-cadherin). CDH11 was broadly expressed in human normal adult and fetal tissues, while its silencing and promoter CpG methylation were frequently detected in tumor cell lines, but not in immortalized normal epithelial cells. Aberrant methylation was also frequently detected in multiple primary tumors. CDH11 silencing could be reversed by pharmacologic or genetic demethylation, indicating an epigenetic mechanism. Ectopic expression of CDH11 strongly suppressed tumorigenecity and induced tumor cell apoptosis. Moreover, CDH11 was found to inhibit Wnt/β-catenin and AKT/Rho A signaling, as well as actin stress fiber formation, thus further inhibiting tumor cell migration and invasion. CDH11 also inhibited epithelial-to-mesenchymal transition and downregulated stem cell markers. Thus, our work identifies CDH11 as a functional tumor suppressor and an important antagonist of Wnt/β-catenin and AKT/Rho A signaling, with frequent epigenetic inactivation in common carcinomas.Oncogene advance online publication, 5 December 2011; doi:10.1038/onc.2011.541.

Back-to-back hadron pair yields in d+Au and p+p collisions at √s(NN)=200 GeV were measured with the PHENIX detector at the Relativistic Heavy Ion Collider. Rapidity separated hadron pairs were detected with the trigger hadron at pseudorapidity |η|<0.35 and the associated hadron at forward rapidity (deuteron direction, 3.0<η<3.8). Pairs were also detected with both hadrons measured at forward rapidity; in this case, the yield of back-to-back hadron pairs in d+Au collisions with small impact parameters is observed to be suppressed by a factor of 10 relative to p+p collisions. The kinematics of these pairs is expected to probe partons in the Au nucleus with a low fraction x of the nucleon momenta, where the gluon densities rise sharply. The observed suppression as a function of nuclear thickness, p(T), and η points to cold nuclear matter effects arising at high parton densities.

We present measurements of J/ψ yields in d+Au collisions at sqrt[s(NN)]=200  GeV recorded by the PHENIX experiment and compare them with yields in p+p collisions at the same energy per nucleon-nucleon collision. The measurements cover a large kinematic range in J/ψ rapidity (-2.2<y<2.4) with high statistical precision and are compared with two theoretical models: one with nuclear shadowing combined with final state breakup and one with coherent gluon saturation effects. In order to remove model dependent systematic uncertainties we also compare the data to a simple geometric model. The forward rapidity data are inconsistent with nuclear modifications that are linear or exponential in the density weighted longitudinal thickness, such as those from the final state breakup of the bound state.

Using genome-wide methylation screening, we identified that paired box gene 5 (PAX5) is involved in human cancer development. However, the function of PAX5 in gastric cancer (GC) development is largely unclear. We analyzed its epigenetic inactivation, biological functions and clinical application in GC. PAX5 was silenced in seven out of eight GC cell lines. A significant downregulation was also detected in paired gastric tumors compared with adjacent non-cancerous tissues. The downregulation of PAX5 was closely linked to the promoter hypermethylation status and could be restored with demethylation treatment. Ectopic expression of PAX5 in silenced GC cell lines (AGS and BGC823) inhibited colony formation and cell viability, arrested cell cycle, induced apoptosis, suppressed cell migration and invasion and repressed tumorigenicity in nude mice. Consistent with the induction of apoptosis by PAX5 in vitro, terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) staining showed significantly enhanced apoptotic cells in PAX5-expressed tumors compared with the vector control tumors. On the other hand, knockdown of PAX5 by PAX5-short hairpin RNA increased the cell viability and proliferation. The anti-tumorigenic function of PAX5 was revealed to be mediated by upregulating downstream targets of tumor protein 53 (p53), p21, BCL2-associated X protein, metastasis suppressor 1 and tissue inhibitors of metalloproteinase 1, and downregulating BCL2, cyclin D1, mesenchymal-epithelial transition factor (MET) and matrix metalloproteinase 1. Immunoprecipitation assay demonstrated that PAX5 directly bound to the promoters of p53 and MET. Moreover, PAX5 hypermethylation was detected in 77%(144 of 187) of primary GCs compared with 10.5%(2/19) of normal gastric tissues (P<0.0001). GC patients with PAX5 methylation had a significant poor survival compared with the unmethylated cases as demonstrated by Cox regression model and log-rank test. In conclusion, PAX5 is a novel functional tumor suppressor in gastric carcinogenesis. Detection of methylated PAX5 can be utilized as an independent prognostic factor in GC.Oncogene advance online publication, 21 November 2011; doi:10.1038/onc.2011.511.