Hardware and software co-simulation platform for convolution or correlation based image processing algorithms

Software implementation of image processing algorithms in which convolution or correlation is applied is too slow to be real-time. As long as the system design gets larger, it should be partitioned into two parts: software and hardware. In order to achieve real time performance, it is essential to map the fast convolution or correlation module, which is the heaviest computation intensive part, in hardware instead of software. Our test case is “generic image pre-processing algorithm” which includes resizing, noise filtering and normalization. In noise filtering part of the preprocessing algorithm in which convolution is used should be implemented in hardware while the rest of the preprocessing algorithm stays in software. Next, to verify our hardware/design software we can deploy it on FPGA board, but it is very time consuming and involves a lot of technical complexities. In that case, this design used hardware/software co-simulation and direct programming interface (DPI-C) whereas it allows System Verilog calls C functions and vice versa. The proposed work has overcome the problems faced when running a co-simulation based on Modelsim simulated using direct programming interface (DPI) technique

Molecular genetic studies in pregnancies affected by preeclampsia and intrauterine growth restriction

Preeclampsia and fetal growth restriction (FGR) are common and costly obstetric complications. Both conditions are associated with immediate and remote mortality and morbidity for the mother and the offspring. Impaired placentation and aberrant maternal systemic responses are implicated as pathophysiological mechanisms in preeclampsia and FGR. Both preeclampsia and FGR are known to have a clear genetic basis. This study has investigated the roles of several candidate genes including those previously associated with diabetes (TCF7L2, FTO, PPAR-g, CDKN2B-AS1 and KCNJ11), and epidermal growth factor (EGF). Functional consequences of variants within the EGF gene were also investigated. A bidirectional association between type 2 diabetes (T2D) and preeclampsia is consistently reported, whereby each condition is associated with an increased risk of the other. Furthermore, fetal growth restriction, which complicates 30% of preeclamptic pregnancies, predisposes the offspring to an increased risk of type 2 diabetes and coronary artery disease (CAD) later in life. 11 single nucleotide polymorphisms (SNPs) reproducibly associated with T2D in the TCF7L2, FTO, PPAR-y, CDKN2B-AS1 and KCNJ11 genes were investigated as susceptibility loci for preeclampsia and fetal growth restriction in a maternal case control study. The study group consisted of 448 white western European women with preeclampsia, 673 controls with no evidence of preeclampsia, 243 women with pregnancies complicated by FGR, and 570 controls with no evidence of growth restriction. A maternal haplotype on the T2D region of the CDKN2BAS1 gene on chromosome 9p21 was found to be a risk variant for fetal growth restriction (P=O.005).The other 9 investigated SNPs in TCF7L2, FTO, PPAR-y, and KCNJ11 showed no association with growth restricted pregnancies. None of the SNPs investigated showed an association with preeclampsia. These findings suggest that some maternal diabetogenic risk variants are associated with an altered risk of FGR pregnancy but not preeclampsia. The results require replication in a larger sample and fetal-maternal gene interactions merit investigation. Epidermal growth factor (EGF) is described as a major regulator of the placentation process. It also helps to maintain an adequate blood supply to the growing fetus through its effects on umbilical vessel tone. Investigating the role of two genetic variants of the EGF gene in susceptibility to preeclampsia and FGR showed that the maternal variants, rs4444903 in the 5'UTR and rs2237051 in exon 14 of the EGF gene has no effect on the risk of preeclampsia or FGR pregnancy. The G allele of the SNP rs4444903 was associated with higher systolic blood pressure measures in the control group. The G allele of the rs4444903 and the A allele of rs2237051 have been associated with increased risk for FGR and lower birth weight in a previous study from our laboratory. This led to investigations to characterize the functional consequences of the two SNPs in the EGF gene on transcription, translation and ribonucleic acid (RNA) splicing using a variety of methods. These experiments have shown that the G allele of rs4444903 was transcriptionally more active than the A allele in hepatocellular carcinoma (HepG2) and more active than EGFP on its own in choriocarcinoma (Jeg-3) cell lines using a luciferase reporter gene assay. There was no effect of this variant on translational efficiency in the cell lines investigated using reporter gene assays, or in a cell free environment using an in vitro translation assay. DNA-protein interaction was investigated using nuclear extract from HepG2 cells to further define the mechanism by which the G allele exerts its higher transcriptional activity. Initial experiments suggest that the Sp1 transcription factor interacts with and represses the A allele of the rs4444903 SNP. The study also demonstrated no evidence of higher activity of the G allele on EGF expression in vivo using term placental tissues. It was expected that higher EGF expression as a function of genotype at rs4444903 SNP may lead to down regulation of the EGFR in the placenta, which was not confirmed in this study. SNP rs2237051 in exon 14 of the EGF gene is in strong linkage disequilibrium with rs4444903, and disrupts a predicted exon splicing enhancer region. This polymorphism was investigated using a minigene assay, but there was no evidence that it affected splicing of exon 14. Taken together, these findings provide no evidence that EGF genetic variants alter the risk of preeclampsia or FGR though functioning

Stochastic Computing Correlation Utilization in Convolutional Neural Network Basic Functions

In recent years, many applications have been implemented in embedded systems and mobile Internet of Things (IoT) devices that typically have constrained resources, smaller power budget, and exhibit "smartness" or intelligence. To implement computation-intensive and resource-hungry Convolutional Neural Network (CNN) in this class of devices, many research groups have developed specialized parallel accelerators using Graphical Processing Units (GPU), Field-Programmable Gate Arrays (FPGA), or Application-Specific Integrated Circuits (ASIC). An alternative computing paradigm called Stochastic Computing (SC) can implement CNN with low hardware footprint and power consumption. To enable building more efficient SC CNN, this work incorporates the CNN basic functions in SC that exploit correlation, share Random Number Generators (RNG), and is more robust to rounding error. Experimental results show our proposed solution provides significant savings in hardware footprint and increased accuracy for the SC CNN basic functions circuits compared to previous work

Molecular genetic studies in pregnancies affected by preeclampsia and intrauterine growth restriction

Preeclampsia and fetal growth restriction (FGR) are common and costly obstetric complications. Both conditions are associated with immediate and remote mortality and morbidity for the mother and the offspring. Impaired placentation and aberrant maternal systemic responses are implicated as pathophysiological mechanisms in preeclampsia and FGR. Both preeclampsia and FGR are known to have a clear genetic basis. This study has investigated the roles of several candidate genes including those previously associated with diabetes (TCF7L2, FTO, PPAR-g, CDKN2B-AS1 and KCNJ11), and epidermal growth factor (EGF). Functional consequences of variants within the EGF gene were also investigated. A bidirectional association between type 2 diabetes (T2D) and preeclampsia is consistently reported, whereby each condition is associated with an increased risk of the other. Furthermore, fetal growth restriction, which complicates 30% of preeclamptic pregnancies, predisposes the offspring to an increased risk of type 2 diabetes and coronary artery disease (CAD) later in life. 11 single nucleotide polymorphisms (SNPs) reproducibly associated with T2D in the TCF7L2, FTO, PPAR-y, CDKN2B-AS1 and KCNJ11 genes were investigated as susceptibility loci for preeclampsia and fetal growth restriction in a maternal case control study. The study group consisted of 448 white western European women with preeclampsia, 673 controls with no evidence of preeclampsia, 243 women with pregnancies complicated by FGR, and 570 controls with no evidence of growth restriction. A maternal haplotype on the T2D region of the CDKN2BAS1 gene on chromosome 9p21 was found to be a risk variant for fetal growth restriction (P=O.005).The other 9 investigated SNPs in TCF7L2, FTO, PPAR-y, and KCNJ11 showed no association with growth restricted pregnancies. None of the SNPs investigated showed an association with preeclampsia. These findings suggest that some maternal diabetogenic risk variants are associated with an altered risk of FGR pregnancy but not preeclampsia. The results require replication in a larger sample and fetal-maternal gene interactions merit investigation. Epidermal growth factor (EGF) is described as a major regulator of the placentation process. It also helps to maintain an adequate blood supply to the growing fetus through its effects on umbilical vessel tone. Investigating the role of two genetic variants of the EGF gene in susceptibility to preeclampsia and FGR showed that the maternal variants, rs4444903 in the 5'UTR and rs2237051 in exon 14 of the EGF gene has no effect on the risk of preeclampsia or FGR pregnancy. The G allele of the SNP rs4444903 was associated with higher systolic blood pressure measures in the control group. The G allele of the rs4444903 and the A allele of rs2237051 have been associated with increased risk for FGR and lower birth weight in a previous study from our laboratory. This led to investigations to characterize the functional consequences of the two SNPs in the EGF gene on transcription, translation and ribonucleic acid (RNA) splicing using a variety of methods. These experiments have shown that the G allele of rs4444903 was transcriptionally more active than the A allele in hepatocellular carcinoma (HepG2) and more active than EGFP on its own in choriocarcinoma (Jeg-3) cell lines using a luciferase reporter gene assay. There was no effect of this variant on translational efficiency in the cell lines investigated using reporter gene assays, or in a cell free environment using an in vitro translation assay. DNA-protein interaction was investigated using nuclear extract from HepG2 cells to further define the mechanism by which the G allele exerts its higher transcriptional activity. Initial experiments suggest that the Sp1 transcription factor interacts with and represses the A allele of the rs4444903 SNP. The study also demonstrated no evidence of higher activity of the G allele on EGF expression in vivo using term placental tissues. It was expected that higher EGF expression as a function of genotype at rs4444903 SNP may lead to down regulation of the EGFR in the placenta, which was not confirmed in this study. SNP rs2237051 in exon 14 of the EGF gene is in strong linkage disequilibrium with rs4444903, and disrupts a predicted exon splicing enhancer region. This polymorphism was investigated using a minigene assay, but there was no evidence that it affected splicing of exon 14. Taken together, these findings provide no evidence that EGF genetic variants alter the risk of preeclampsia or FGR though functioning

A Low-complexity Complex-valued Activation Function for Fast and Accurate Spectral Domain Convolutional Neural Network

Conventional Convolutional Neural Networks (CNNs), which are realized in spatial domain, exhibit high computational complexity. This results in high resource utilization and memory usage and makes them unsuitable for implementation in resource and energy-constrained embedded systems. A promising approach for low-complexity and high-speed solution is to apply CNN modeled in the spectral domain. One of the main challenges in this approach is the design of activation functions. Some of the proposed solutions perform activation functions in spatial domain, necessitating multiple and computationally expensive spatial-spectral domain switching. On the other hand, recent work on spectral activation functions resulted in very computationally intensive solutions. This paper proposes a complex-valued activation function for spectral domain CNNs that only transmits input values that have positive-valued real or imaginary component. This activation function is computationally inexpensive in both forward and backward propagation and provides sufficient nonlinearity that ensures high classification accuracy. We apply this complex-valued activation function in a LeNet-5 architecture and achieve an accuracy gain of up to 7% for MNIST and 6% for Fashion MNIST dataset, while providing up to 79% and 85% faster inference times, respectively, over state-of-the-art activation functions for spectral domain

Association between Type 2 diabetes mellitus and TCF7L2 and FTO gene variants among upper Egyptian population

Background: Type 2 diabetes mellitus (T2DM) is a metabolic disorder caused by a complex interaction of genetic and environmental variables. T2DM is associated with transcription factor 7-like 2 (TCF7L2) and fat mass and obesity-associated (FTO) genetic polymorphism.Objectives: The goal of this study was to examine the common genetic risk factors of T2DM and related metabolic traits in Upper Egyptian population, in attempt to understand the genetic structure of T2DM in the Egyptian community.Methods and Materials: This case control study included 250 participants, 124 T2DM patients and 126 non-diabetics. Using mutagenically separated polymerase chain reaction (MS-PCR), genotyping of single nucleotide polymorphisms (SNP) rs7903146 of TCF7L2 and rs17817449 of FTO genes was carried out.Results: T allele of TCF7L2 variant rs7903146 confers a risk for T2DM (allelic OR=1.97, 95% CI: (1.34 to 2.88) p =<0.001). The minor G allele of FTO rs17817449 polymorphism was significantly higher in diabetics than controls (allelic OR=1.87, 95% CI=1.30 to 2.68, p<0.001). Genotype risk was evident under both recessive and dominant modes of inheritance (OR=3.18, CI (1.35-7.45), P =0.008, OR= 2.04, CI (1.23-3.38), p=0.006) for TCF7L2 and (OR= 2.55, CI (1.28 -5.09), p=0.008 and OR= 2.14, CI (1.25-3.63), p= 0.005) for FTO respectivelyConclusion: TCF7L2 rs7903146 and FTO rs17817449 variant conferred risk for T2DM in Upper Egyptian population. The study noted the interaction between certain biological and environmental risk factors including BMI, age, and sex and the conferred genetic risk

Clinical and genetic assessment of pediatric patients with Gaucher’s disease in Upper Egypt

Background: Gaucher’s disease (GD) is an autosomal recessive genetic disorder that results from pathogenic mutations of GBA gene encoding the enzyme glucocerebrosidase (acid b-glucosidase). Of the approximately 300 mutations associated with GD, 4 accounts for the majority of mutations seen in GD patients: N370S, L444P, 84 GG and IVS2+1.Aim: Establishing and providing, clinical and molecular backgrounds of pediatric patients with GD in Upper Egypt.Subjects and methods: The present study is a cross sectional study, carried out on 26 pediatric patients with GD. They were recruited from the pediatric outpatient clinics and inpatients Pediatric departments of Assiut and Qena University hospitals, Upper Egypt. Clinical evaluation and mutation analysis using commercially available strip assay kit after PCR amplification of the target gene were done for all included GD patients.Results: Consanguinity between patients’ parents was present in 73.1% of the included patients. 76.9% of included patients were of type 1 GD, while 23.1% were of type 3 GD and none of our patients was classified as type 2 GD. The main frequent clinical presentations of GD in this study were hepatosplenomegaly (88.5%); pallor (76.9%); abdominal distension (61.5%) and musculoskeletal involvement (37.1%). Neurological abnormalities of type 3 GD included in this study were squint, seizures and delayed mental development. Five different genotypes were detected, homozygous for the mutation L444P, homozygous for the mutation N370S, heterozygous for the mutations N370S and rec Ncil, heterozygous for IVS2 +1 and rec NciI, heterozygous for L444P and IVS2 +1. Conclusions: Non-neuropathic type 1 and type 3 GD were the only clinical types found in the present study. The most common mutant alleles found in this study were L444P and N370S

Causes of elective cesarean delivery on maternal request in Aljouf, Saudi Arabia

Background: Recently observed there is a steadily higher rate of cesarean delivery worldwide mostly due to the increasing number of women requesting an elective cesarean section on maternal request without valid indication. The aim of the study was to determine the causes of elective cesarean delivery on maternal requests in Aljouf Saudi Arabia.Methods: This was a descriptive cross-sectional study and data was evaluated by completing seven questionnaires and interviews with laboratory reports who were admitted for cesarean delivery at the Obstetrics department of Maternity and Children Hospital (MCH) Aljouf, Saudi Arabia from January 2020 to December 2020. A total of 141 Saudi women of age between 18 and over 35 years were enrolled, including those who have singleton pregnancy, no complications during pregnancy, and no medical indication for cesarean delivery.Results: 141 women reported willingness to request cesarean delivery. The mean systolic 120±6.23, diastolic 75±2.45 blood pressure mm of Hg, and fasting blood sugar level 4.1±1.1 mmol/l have been found within the normal limit. The ultrasound (US) confirmed singleton pregnancy without any abnormalities.  Data reveals that common causes of elective cesarean section on maternal request to avoid the episiotomy 77.3%, fear of labor pain 69.5%, trauma to the vagina 79.4%, uncertainty about timing 61.7%, losing a baby during vaginal delivery 54.6%, experience other members 41.8%, the risk for baby 39%, prolapse or incontinence24.1%, unsatisfactory sexual intercourse 17.7% and the undesirable experience of the previous vaginal delivery 12%.Conclusions: Maternal request for cesarean delivery is considered one of the reasons for increasing the rate of cesarean delivery in Saudi Arabia. To avoid the episiotomy and fear of labor pain may strong causes for choosing cesarean delivery

Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis

BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London