Interference Cancellation trough Interference Alignment for Downlink of Cognitive Cellular Networks

In this letter, we propose the interference cancellation through interference alignment at the downlink of cognitive cellular networks. Interference alignment helps the spatial resources to be shared among primary and secondary cells and thus, it can provide higher degrees of freedom through interference cancellation. We derive and depict the achievable degrees of freedom. We also analyse and calculate the achievable sum rates applying water-filling optimal power allocation

A Role for Fetal Hemoglobin and Maternal Immune IgG in Infant Resistance to Plasmodium falciparum Malaria

In Africa, infant susceptibility to Plasmodium falciparum malaria increases substantially as fetal hemoglobin (HbF) and maternal immune IgG disappear from circulation. During the first few months of life, however, resistance to malaria is evidenced by extremely low parasitemias, the absence of fever, and the almost complete lack of severe disease. This resistance has previously been attributed in part to poor parasite growth in HbF-containing red blood cells (RBCs). A specific role for maternal immune IgG in infant resistance to malaria has been hypothesized but not yet identified.We found that P. falciparum parasites invade and develop normally in fetal (cord blood, CB) RBCs, which contain up to 95% HbF. However, these parasitized CB RBCs are impaired in their binding to human microvascular endothelial cells (MVECs), monocytes, and nonparasitized RBCs--cytoadherence interactions that have been implicated in the development of high parasite densities and the symptoms of malaria. Abnormal display of the parasite's cytoadherence antigen P. falciparum erythrocyte membrane protein-1 (PfEMP-1) on CB RBCs accounts for these findings and is reminiscent of that on HbC and HbS RBCs. IgG purified from the plasma of immune Malian adults almost completely abolishes the adherence of parasitized CB RBCs to MVECs.Our data suggest a model of malaria protection in which HbF and maternal IgG act cooperatively to impair the cytoadherence of parasitized RBCs in the first few months of life. In highly malarious areas of Africa, an infant's contemporaneous expression of HbC or HbS and development of an immune IgG repertoire may effectively reconstitute the waning protective effects of HbF and maternal immune IgG, thereby extending the malaria resistance of infancy into early childhood

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

A first update on mapping the human genetic architecture of COVID-19

peer reviewe

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Post-permeation stability of modified bentonite suspensions under increasing hydraulic gradients

textSlurry wall is a geotechnical engineering application to control the migration of contaminants by retarding groundwater flow. Sand-bentonite slurry walls are commonly used as levees and containment liners. The performance of bentonite slurry in sand-bentonite slurry walls was investigated by studying the rheological properties of bentonite suspensions, the penetration length of bentonite slurry into clean sand, and stability of the trench under in-situ hydraulic gradients. In this study, the rheological parameters of bentonite suspensions were measured at various bentonite fractions by weight from 6 to 12% with 0-3% of sodium pyrophosphate; an ionic additive to control the rheological properties of the bentonite slurries. The penetrability of the bentonite slurries through Ottawa sand was studied by injecting the slurries into sand columns at different bentonite fractions. The injection tests were performed with the permeameters having different diameters to eliminate any bias on test results due to the different size of permeameter. An empirical correlation for predicting the penetration length of bentonite slurry based on apparent viscosity, yield stress, effective particle size, relative density, and injection pressures was updated by taking into account the effects of the permeameter diameter size. Moreover, the stability of sand-bentonite slurry walls was inspected by studying the hydraulic performance of sand permeated with bentonite suspensions under increasing hydraulic gradients. The critical hydraulic gradient at which washing out of bentonite suspensions is initiated was examined. For specimens with bentonite contents less than the threshold value, the flow occurred through the sand voids and minimal washing out occurred. On the other hand, when the bentonite content was high enough to fill up all the void space between the sand particles, the flow was controlled by the clay void ratio. In this case, washing out did occur with increasing gradients accompanied by an increase in hydraulic conductivity. Accordingly, a relation between the yield stress of bentonite suspensions and the critical hydraulic conductivity was developed.Civil, Architectural, and Environmental Engineerin

A critical study and edition of Sharh al-Makkudi 'Ala Alfiyyat Ibn Malik by Abu Zaid al-Makkudi (d. 807 AH/1405 CE)

The researcher has examined more than sixty manuscript but he has chosen five copies of them for study and edition. The research deals with the emergence of Arabic Grammar and its development up to the time of Ibn Mālik the writer of the Alfiyyah who died in 672AH / 1274CE. The research also concentrates on the study of the era of al-Makkūdī which covers aspects of political, social, economic and religious life, with a special emphasis on cultural life and general scientific environment. It discusses the life of al-Makkūdī covering different areas such as his family, birth, childhood, teachers, scientific activity, poetic abilities, students, death and finally his works of which his Commentary on the Alfiyyah is the most important. It also reviews the study al-Makkūdī’s commentary covering the title, the date of composition, sources used and the method adopted by al-Makkūdī. The thesis gives details of the some of the works produced about the Commentary. Finally the thesis introduces many copies of the manuscript from various libraries around the world, detailing their degree of completion and diminution, dates of scribing, names of scribes, the number of pages, the style of writing. It focuses on giving a detailed description of the selected copies; five copies were chosen for the research four were manuscripts and the fifth an old stone printed copy (TabCah Hajariyyah).EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Expression of Plasmodium falciparum 3D7 STEVOR proteins for evaluation of antibody responses following malaria infections in naïve infants

Clinical immunity to Plasmodium falciparum malaria develops after repeated exposure to the parasite. At least 2 P. falciparum variant antigens encoded by multicopy gene families (var and rif) are targets of this adaptive antibody-mediated immunity. A third multigene family of variant antigens comprises the stevor genes. Here, 4 different stevor sequences were selected for cloning and expression in Escherichia coli and His6-tagged fusion proteins were used for assessing the development of immunity. In a cross-sectional analysis of clinically immune adults living in a malaria endemic area in Ghana, high levels of anti-STEVOR IgG antibody titres were determined in ELISA. A cross-sectional study of 90 nine-month-old Ghanaian infants using 1 recombinant STEVOR showed that the antibody responses correlated positively with the number of parasitaemia episodes. In a longitudinal investigation of 17 immunologically naïve 9-month-old infants, 3 different patterns of anti-STEVOR antibody responses could be distinguished (high, transient and low). Children with high anti-STEVOR-antibody levels exhibited an elevated risk for developing parasitaemia episodes. Overall, a protective effect could not be attributed to antibodies against the STEVOR proteins chosen for the study presented here