The Complete Mitochondrial Genome Sequence of the Planthopper, Sivaloka damnosus

The complete mitochondrial genome (mitogenome) sequence was determined from the plant hopper, Sivaloka damnosus Chow and Lu (Hemiptera: Issidae), a representative of the insect family Issidae. The genome is a circular molecule of 15,287 bp with a total A+T content of 76.5%. The gene content, order, and structure are identical to that in Drosophila melanogaster, which is considered ancestral for insects. All 13 protein-coding genes of the S. damnosus mitogenome have a putative inframe ATR methionine or ATT isoleucine codons as start signals. The usual termination codons (TAA and TAG) were found in 11 protein-coding genes. However, atp6, and nad4 have incomplete termination codons. All tRNAs show stable canonical clover-leaf structures similar to other insect mitochondrial tRNAs, except for tRNASer(AGN), which has a reduced DHU arm. The A+T-rich region or putative control region includes two extensive repeat regions. The first repeat region is composed of two sets of complicated repeat units, and these repetitive sequences are arranged alternately; the second contains ten 20 bp tandemly repetitive sequences. In the phylogenetic analyses based on protein-coding genes, Cicadomorpha is a sister to Fulgoromorpha+Sternorrhyncha, and Heteroptera is a sister to all other Hemiptera

Adiposity has differing associations with incident coronary heart disease and mortality in the Scottish population: cross-sectional surveys with follow-up

Objective: Investigation of the association of excess adiposity with three different outcomes: all-cause mortality, coronary heart disease (CHD) mortality and incident CHD. Design: Cross-sectional surveys linked to hospital admissions and death records. Subjects: 19 329 adults (aged 18–86 years) from a representative sample of the Scottish population. Measurements: Gender-stratified Cox proportional hazards models were used to estimate hazard ratios (HRs) for all-cause mortality, CHD mortality and incident CHD. Separate models incorporating the anthropometric measurements body mass index (BMI), waist circumference (WC) or waist–hip ratio (WHR) were created adjusted for age, year of survey, smoking status and alcohol consumption. Results: For both genders, BMI-defined obesity (greater than or equal to30 kg m−2) was not associated with either an increased risk of all-cause mortality or CHD mortality. However, there was an increased risk of incident CHD among the obese men (hazard ratio (HR)=1.78; 95% confidence interval=1.37–2.31) and obese women (HR=1.93; 95% confidence interval=1.44–2.59). There was a similar pattern for WC with regard to the three outcomes; for incident CHD, the HR=1.70 (1.35–2.14) for men and 1.71 (1.28–2.29) for women in the highest WC category (men greater than or equal to102 cm, women greater than or equal to88 cm), synonymous with abdominal obesity. For men, the highest category of WHR (greater than or equal to1.0) was associated with an increased risk of all-cause mortality (1.29; 1.04–1.60) and incident CHD (1.55; 1.19–2.01). Among women with a high WHR (greater than or equal to0.85) there was an increased risk of all outcomes: all-cause mortality (1.56; 1.26–1.94), CHD mortality (2.49; 1.36–4.56) and incident CHD (1.76; 1.31–2.38). Conclusions: In this study excess adiposity was associated with an increased risk of incident CHD but not necessarily death. One possibility is that modern medical intervention has contributed to improved survival of first CHD events. The future health burden of increased obesity levels may manifest as an increase in the prevalence of individuals living with CHD and its consequences

A deletion of FGFR2 creating a chimeric IIIb/IIIc exon in a child with Apert syndrome

<p>Abstract</p> <p>Background</p> <p>Signalling by fibroblast growth factor receptor type 2 (FGFR2) normally involves a tissue-specific alternative splice choice between two exons (IIIb and IIIc), which generates two receptor isoforms (FGFR2b and FGFR2c respectively) with differing repertoires of FGF-binding specificity. Here we describe a unique chimeric IIIb/c exon in a patient with Apert syndrome, generated by a non-allelic homologous recombination event.</p> <p>Case Presentation</p> <p>We present a child with Apert syndrome in whom routine genetic testing had excluded the <it>FGFR2 </it>missense mutations commonly associated with this disorder. The patient was found to harbour a heterozygous 1372 bp deletion between <it>FGFR2 </it>exons IIIb and IIIc, apparently originating from recombination between 13 bp of identical DNA sequence present in both exons. The rearrangement was not present in the unaffected parents.</p> <p>Conclusions</p> <p>Based on the known pathogenesis of Apert syndrome, the chimeric FGFR2 protein is predicted to act in a dominant gain-of-function manner. This is likely to result from its expression in mesenchymal tissues, where retention of most of the residues essential for FGFR2b binding activity would result in autocrine activation. This report adds to the repertoire of rare cases of Apert syndrome for which a pathogenesis based on atypical <it>FGFR2 </it>rearrangements can be demonstrated.</p

Extraordinary carrier multiplication gated by a picosecond electric field pulse

The study of carrier multiplication has become an essential part of many-body physics and materials science as this multiplication directly affects nonlinear transport phenomena, and has a key role in designing efficient solar cells and electroluminescent emitters and highly sensitive photon detectors. Here we show that a 1-MVcm−1 electric field of a terahertz pulse, unlike a DC bias, can generate a substantial number of electron–hole pairs, forming excitons that emit near-infrared luminescence. The bright luminescence associated with carrier multiplication suggests that carriers coherently driven by a strong electric field can efficiently gain enough kinetic energy to induce a series of impact ionizations that can increase the number of carriers by about three orders of magnitude on the picosecond time scale

Management of Hepatic Angiomyolipoma

Preoperative diagnosis of hepatic angiomyolipoma is difficult, and the treatment for it remains controversial. The aim of this study is to review our experience in the treatment of hepatic angiomyolipoma and to propose a treatment strategy for this disease. We retrospectively collected the clinical, imaging, and pathological features of patients with hepatic angiomyolipoma. Immunohistochemical studies with antibodies for HMB-45, actin, S-100, cytokeratin, vimentin, and c-kit were performed. Treatment experience and long-term follow-up results are summarized. During a period of 9 years, 10 patients with hepatic angiomyolipoma were treated at our hospital. There was marked female predominance (nine patients). Nine patients received surgical resection without complications. One patient received nonoperative management with biopsy and follow-up. One patient died 11 months after surgery because of recurrent disease. We propose all symptomatic patients should receive surgical resection for hepatic angiomyolipoma. Conservative management with close follow-up is suggested in patients with asymptomatic tumors and meet the following criteria: (1) tumor size smaller than 5 cm, (2) angiomyolipoma proved through fine needle aspiration biopsy, (3) patients with good compliance, and (4) not a hepatitis virus carrier

Pseudo-acetylation of multiple sites on human Tau proteins alters Tau phosphorylation and microtubule binding, and ameliorates amyloid beta toxicity

Tau is a microtubule-associated protein that is highly soluble and natively unfolded. Its dysfunction is involved in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD), where it aggregates within neurons. Deciphering the physiological and pathogenic roles of human Tau (hTau) is crucial to further understand the mechanisms leading to its dysfunction in vivo. We have used a knock-out/knock-in strategy in Drosophila to generate a strain with hTau inserted into the endogenous fly tau locus and expressed under the control of the endogenous fly tau promoter, thus avoiding potential toxicity due to genetic over-expression. hTau knock-in (KI) proteins were expressed at normal, endogenous levels, bound to fly microtubules and were post-translationally modified, hence displaying physiological properties. We used this new model to investigate the effects of acetylation on hTau toxicity in vivo. The simultaneous pseudo-acetylation of hTau at lysines 163, 280, 281 and 369 drastically decreased hTau phosphorylation and significantly reduced its binding to microtubules in vivo. These molecular alterations were associated with ameliorated amyloid beta toxicity. Our results indicate acetylation of hTau on multiple sites regulates its biology and ameliorates amyloid beta toxicity in vivo

A Study of B0 -> J/psi K(*)0 pi+ pi- Decays with the Collider Detector at Fermilab

We report a study of the decays B0 -> J/psi K(*)0 pi+ pi-, which involve the creation of a u u-bar or d d-bar quark pair in addition to a b-bar -> c-bar(c s-bar) decay. The data sample consists of 110 1/pb of p p-bar collisions at sqrt{s} = 1.8 TeV collected by the CDF detector at the Fermilab Tevatron collider during 1992-1995. We measure the branching ratios to be BR(B0 -> J/psi K*0 pi+ pi-) = (8.0 +- 2.2 +- 1.5) * 10^{-4} and BR(B0 -> J/psi K0 pi+ pi-) = (1.1 +- 0.4 +- 0.2) * 10^{-3}. Contributions to these decays are seen from psi(2S) K(*)0, J/psi K0 rho0, J/psi K*+ pi-, and J/psi K1(1270)

CD133-positive hepatocellular carcinoma in an area endemic for hepatitis B virus infection

<p>Abstract</p> <p>Background</p> <p>CD133 was detected in several types of cancers including hepatocellular carcinoma (HCC), which raised the possibility of stem cell origin in a subset of cancers. However, reappearance of embryonic markers in de-differentiated malignant cells was commonly observed. It remained to be elucidated whether CD133-positive HCCs were indeed of stem cell origin or they were just a group of poorly differentiated cells acquiring an embryonic marker. The aim of this study was to investigate the significance of CD133 expression in HCC in an area endemic for hepatitis B virus (HBV) infection to gain insights on this issue.</p> <p>Methods</p> <p>154 HCC patients receiving total removal of HCCs were included. 104 of them (67.5%) were positive for HBV infection. The cancerous and adjacent non-cancerous liver tissues were subjected for Western blot and immunohistochemistry analysis for CD133 expression. The data were correlated with clinical parameters, patient survivals, and p53 expression.</p> <p>Results</p> <p>Of 154 patients, 24 (15.6%) had CD133 expression in HCC. Univariate and multivariate logistic regression analysis revealed that CD133 expression was negatively correlated with the presence of hepatitis B surface antigen (HBsAg). The unadjusted and adjusted odds ratios were 0.337 (95%CI 0.126 - 0.890) and 0.084 (95%CI 0.010 - 0.707), respectively. On the other hand, p53 expression was positively associated with the presence of HBsAg in univariate analysis. The unadjusted odds ratio was 4.203 (95%CI 1.110 - 18.673). Survival analysis indicated that both CD133 and p53 expression in HCC predicted poor disease-free survival (P = 0.009 and 0.001, respectively), whereas only CD133 expression predicted poor overall survival (P = 0.001). Cox proportional hazard model showed that p53 and CD133 expression were two independent predictors for disease-free survival. The hazard ratios were 1.697 (95% CI 1.318 - 2.185) and 2.559 (95% CI 1.519 - 4.313), respectively (P < 0.001 for both).</p> <p>Conclusion</p> <p>In area where HBV infection accounts for the major attributive risk of HCC, CD133 expression in HCC was negatively associated with the presence of HBsAg, implicating a non-viral origin of CD133-positive HCC. Additionally, CD133 expression predicted poor disease-free survival independently of p53 expression, arguing for two distinguishable hepatocarcinogenesis pathways.</p

Reduced Physiological Complexity in Robust Elderly Adults with the APOE ε4 Allele

BACKGROUND:It is unclear whether the loss of physiological complexity during the aging process is due to genetic variations. The APOE gene has been studied extensively in regard to its relationship with aging-associated medical illness. We hypothesize that diminished physiological complexity, as measured by heart rate variability, is influenced by polymorphisms in the APOE allele among elderly individuals. METHODOLOGY/PRINCIPAL FINDINGS:A total of 102 robust, non-demented, elderly subjects with normal functions of daily activities participated in this study (97 males and 5 females, aged 79.2+/-4.4 years, range 72-92 years). Among these individuals, the following two APOE genotypes were represented: epsilon4 non-carriers (n = 87, 85.3%) and epsilon4 carriers (n = 15, 14.7%). Multi-scale entropy (MSE), an analysis used in quantifying complexity for nonlinear time series, was employed to analyze heart-rate dynamics. Reduced physiological complexity, as measured by MSE, was significantly associated with the presence of the APOE epsilon4 allele in healthy elderly subjects, as compared to APOE epsilon4 allele non-carriers (24.6+/-5.5 versus 28.9+/-5.2, F = 9.429, p = 0.003, respectively). CONCLUSIONS/SIGNIFICANCE:This finding suggests a role for the APOE gene in the diminished physiological complexity seen in elderly populations

A framework for increasing the value of predictive data-driven models by enriching problem domain characterization with novel features

The need to leverage knowledge through data mining has driven enterprises in a demand for more data. However, there is a gap between the availability of data and the application of extracted knowledge for improving decision support. In fact, more data do not necessarily imply better predictive data-driven marketing models, since it is often the case that the problem domain requires a deeper characterization. Aiming at such characterization, we propose a framework drawn on three feature selection strategies, where the goal is to unveil novel features that can effectively increase the value of data by providing a richer characterization of the problem domain. Such strategies involve encompassing context (e.g., social and economic variables), evaluating past history, and disaggregate the main problem into smaller but interesting subproblems. The framework is evaluated through an empirical analysis for a real bank telemarketing application, with the results proving the benefits of such approach, as the area under the receiver operating characteristic curve increased with each stage, improving previous model in terms of predictive performance.The work of P. Cortez was supported by FCT within the Project Scope UID/CEC/00319/2013. The authors would like to thank the anonymous reviewers for their helpful comments.info:eu-repo/semantics/publishedVersio