HERMITE NUMERICAL METHOD TO ESTIMATE THE RADON AND RADIUM EFFECTS OF THE SOIL IN BARTELLA REGION

The Hermite numerical interpolation method used to estimate and predict the radon and radium concentrations, from some of the experimental measurements made on the soil samples of the Bartella region in Iraq. The results obtained from deductible mathematical method were close to real experimental results. Predicted results are in the range of 80.04–4051.59 Bq/m3radon concentrations and 0.322–17.276 Bq/Kgradium concentrations corresponding to 200-10000 tracks of alpha particles. The maximum errors were less than 0.289 and 1.172 percent for radon and radium concentrations, respectively. The effects of radium and radon radiations estimated of soil in the studied area depend on its concentrations, a higher number of alpha particle tracks mean high radiation concentration, the high radiation will cause human health damage. The values are below 370 Bq/Kg the recommended radium concentration permissible values, by the Organization ащк Economic Cooperation and Development (OECD), the studied area is safe from hazards on health of radium and radon exposure from the soi

Case of corrosion control in a closed cooling system

The cooling system of the food is one of the main essential systems to maintain food quality in the food processing plant. The using of corrosion inhibitor for the cooling systems is a familiar practice to control the corrosion which is happening due to a different kind of parameters like water quality and the type of materials for the cooling system, in this work, the case of adding corrosion and scale inhibitor to a cooling system containing carbon steel and stainless steel and copper was investigated. The inhibitor was mixed of two materials which are (Sodium Tripolyphosphate as a scale inhibitor and Sodium Polyphosphate as a corrosion inhibitor). The results demonstrate that there is an improvement in reducing the corrosion rate for iron after adding the inhibitor, and the copper ions in the solution reduced if the PH values below 9.5

Architecture of Pol II(G) and molecular mechanism of transcription regulation by Gdown1.

Tight binding of Gdown1 represses RNA polymerase II (Pol II) function in a manner that is reversed by Mediator, but the structural basis of these processes is unclear. Although Gdown1 is intrinsically disordered, its Pol II interacting domains were localized and shown to occlude transcription factor IIF (TFIIF) and transcription factor IIB (TFIIB) binding by perfect positioning on their Pol II interaction sites. Robust binding of Gdown1 to Pol II is established by cooperative interactions of a strong Pol II binding region and two weaker binding modulatory regions, thus providing a mechanism both for tight Pol II binding and transcription inhibition and for its reversal. In support of a physiological function for Gdown1 in transcription repression, Gdown1 co-localizes with Pol II in transcriptionally silent nuclei of early Drosophila embryos but re-localizes to the cytoplasm during zygotic genome activation. Our study reveals a self-inactivation through Gdown1 binding as a unique mode of repression in Pol II function

Synpolydactyly and HOXD13 polyalanine repeat: addition of 2 alanine residues is without clinical consequences

<p>Abstract</p> <p>Background</p> <p>Type II syndactyly or synpolydactyly (SPD) is clinically very heterogeneous, and genetically three distinct SPD conditions are known and have been designated as SPD1, SPD2 and SPD3, respectively. SPD1 type is associated with expansion mutations in <it>HOXD13</it>, resulting in an addition of ≥ 7 alanine residues to the polyalanine repeat. It has been suggested that expansions ≤ 6 alanine residues go without medical attention, as no such expansion has ever been reported with the SPD1 phenotype.</p> <p>Methods</p> <p>We describe a large Pakistani and an Indian family with SPD. We perform detailed clinical and molecular analyses to identify the genetic basis of this malformation.</p> <p>Results</p> <p>We have identified four distinct clinical categories for the SPD1 phenotype observed in the affected subjects in both families. Next, we show that a milder foot phenotype, previously described as a separate entity, is in fact a part of the SPD1 phenotypic spectrum. Then, we demonstrate that the phenotype in both families segregates with an identical expansion mutation of 21 bp in <it>HOXD13</it>. Finally, we show that the HOXD13 polyalanine repeat is polymorphic, and the expansion of 2 alanine residues, evident in unaffected subjects of both families, is without clinical consequences.</p> <p>Conclusion</p> <p>It is the first molecular evidence supporting the hypothesis that expansion of ≤ 6 alanine residues in the HOXD13 polyalanine repeat is not associated with the SPD1 phenotype.</p

Congenital cystic eye with multiple dermal appendages: a case report

BACKGROUND: A partial or complete failure in the involution of the primary optic vesicle resulting in the formation of a cyst is an extremely rare anomaly known as congenital cystic eye. The primary optic vesicle is formed but instead of the anterior part of the vesicle involuting to lie in apposition with the posterior part, a cyst persists at birth and replaces the eye. CASE PRESENTATION: We report a case of congenital cystic eye associated with multiple dermal appendages in a 1-day-old female child. This condition presented at birth as a large orbital mass in the left orbit that bulged forwards and stretched the eyelids. No globe or any other ocular structures were identified in the orbit. Multiple dermal appendages were present in the adjacent part of the face below the left orbit and on the upper part of the neck. CONCLUSIONS: Congenital cystic eye is an extremely rare condition and with only 28 previous cases reported in the literature. We present the second case of congenital cystic eye with multiple dermal appendages of the face and neck

Channel Characteristics of MIMO-WLAN Communications at 60GHz for Various Corridors

[[abstract]]A comparison of 4 × 4 multiple-input multiple-output wireless local area network wireless communication characteristics for six different geometrical shapes is investigated. These six shapes include the straight shape corridor with rectangular cross section, the straight shape corridor with arched cross section, the curved shape corridor with rectangular cross section, the curved shape corridor with arched cross section, the L-shape corridor, and the T-shape corridor. The impulse responses of these corridors are computed by applying shooting and bouncing ray/image (SBR/Image) techniques along with inverse Fourier transform. By using the impulse response of these multipath channels, the mean excess delay, root mean square (RMS) delay spread for these six corridors can be obtained. Numerical results show that the capacity for the rectangular cross section corridors is smaller than those for the arched cross section corridors regardless of the shapes. And the RMS delay spreads for the T-and the L-shape corridors are greater than the other corridors.[[notice]]補正完畢[[incitationindex]]SCI[[incitationindex]]EI[[booktype]]紙本[[booktype]]電子

Genetics of callous-unemotional behavior in children

Callous-unemotional behavior (CU) is currently under consideration as a subtyping index for conduct disorder diagnosis. Twin studies routinely estimate the heritability of CU as greater than 50%. It is now possible to estimate genetic influence using DNA alone from samples of unrelated individuals, not relying on the assumptions of the twin method. Here we use this new DNA method (implemented in a software package called Genome-wide Complex Trait Analysis, GCTA) for the first time to estimate genetic influence on CU. We also report the first genome-wide association (GWA) study of CU as a quantitative trait. We compare these DNA results to those from twin analyses using the same measure and the same community sample of 2,930 children rated by their teachers at ages 7, 9 and 12. GCTA estimates of heritability were near zero, even though twin analysis of CU in this sample confirmed the high heritability of CU reported in the literature, and even though GCTA estimates of heritability were substantial for cognitive and anthropological traits in this sample. No significant associations were found in GWA analysis, which, like GCTA, only detects additive effects of common DNA variants. The phrase ‘missing heritability’ was coined to refer to the gap between variance associated with DNA variants identified in GWA studies versus twin study heritability. However, GCTA heritability, not twin study heritability, is the ceiling for GWA studies because both GCTA and GWA are limited to the overall additive effects of common DNA variants, whereas twin studies are not. This GCTA ceiling is very low for CU in our study, despite its high twin study heritability estimate. The gap between GCTA and twin study heritabilities will make it challenging to identify genes responsible for the heritability of CU

Sample size calculation for microarray experiments with blocked one-way design

<p>Abstract</p> <p>Background</p> <p>One of the main objectives of microarray analysis is to identify differentially expressed genes for different types of cells or treatments. Many statistical methods have been proposed to assess the treatment effects in microarray experiments.</p> <p>Results</p> <p>In this paper, we consider discovery of the genes that are differentially expressed among <it>K </it>(> 2) treatments when each set of <it>K </it>arrays consists of a block. In this case, the array data among <it>K </it>treatments tend to be correlated because of block effect. We propose to use the blocked one-way ANOVA <it>F</it>-statistic to test if each gene is differentially expressed among <it>K </it>treatments. The marginal p-values are calculated using a permutation method accounting for the block effect, adjusting for the multiplicity of the testing procedure by controlling the false discovery rate (FDR). We propose a sample size calculation method for microarray experiments with a blocked one-way design. With FDR level and effect sizes of genes specified, our formula provides a sample size for a given number of true discoveries.</p> <p>Conclusion</p> <p>The calculated sample size is shown via simulations to provide an accurate number of true discoveries while controlling the FDR at the desired level.</p