Kinds Of Variants Research Articles

Four novel variants identified in the ACADVL gene causing very-long-chain acyl-coenzyme A dehydrogenase deficiency in four unrelated Chinese families.

Background: The biochemical and genetic characteristics of four very-long-chain acyl-coenzyme A dehydrogenase deficiency (VLCADD) patients, clarifying their pathogenic genetic factors and evaluating the application value of genetic diagnosis in the early diagnosis of VLCADD, are reported and discussed in this article. Methods: Patients underwent blood tandem mass spectrometry (MS/MS), urine gas chromatography (GC/MS), and high-throughput sequencing technology. New variants were analyzed for pathogenicity using bioinformatics software. Swiss-PdbViewer software was used to predict the effect of variants on the structure of the very-long-chain acyl-CoA dehydrogenase (VLCAD) protein. Result: A total of four VLCADD patients were diagnosed. They revealed elevated levels of C14, C14:1, C14:2, C14:1/C2, C14:1/C10, and C14:1/C12:1. Two patients were early-onset neonatal cases and died during infancy and the neonatal period, respectively. Seven kinds of variants were detected, including four novel variants. Bioinformatics software revealed that the variants were harmful, and the Swiss-PdbViewer results suggest that variation affects protein conformation. Conclusion: This study identified four novel ACADVL gene variants. These findings contribute to the understanding of the genetic basis and pathogenesis of VLCADD. Meanwhile, the study enriches the genetic mutation spectrum and the correlation between genotypes and phenotypes of VLCADD, indicating that genetic diagnosis plays an essential role in the early diagnosis and treatment of VLCADD.

Prioritizing genomic variants pathogenicity via DNA, RNA, and protein-level features based on extreme gradient boosting.

Genetic diseases are mostly implicated with genetic variants, including missense, synonymous, non-sense, and copy number variants. These different kinds of variants are indicated to affect phenotypes in various ways from previous studies. It remains essential but challenging to understand the functional consequences of these genetic variants, especially the noncoding ones, due to the lack of corresponding annotations. While many computational methods have been proposed to identify the risk variants. Most of them have only curated DNA-level and protein-level annotations to predict the pathogenicity of the variants, and others have been restricted to missense variants exclusively. In this study, we have curated DNA-, RNA-, and protein-level features to discriminate disease-causing variants in both coding and noncoding regions, where the features of protein sequences and protein structures have been shown essential for analyzing missense variants in coding regions while the features related to RNA-splicing and RBP binding are significant for variants in noncoding regions and synonymous variants in coding regions. Through the integration of these features, we have formulated the Multi-level feature Genomic Variants Predictor (ML-GVP) using the gradient boosting tree. The method has been trained on more than 400,000 variants in the Sherloc-training set from the 6th critical assessment of genome interpretation with superior performance. The method is one of the two best-performing predictors on the blind test in the Sherloc assessment, and is further confirmed by another independent test dataset of de novo variants.

Abstract 2326: Integrating single nucleotide variants (SNVs), copy number alterations (CNAs), and structural variants (SVs) into single-cell clonal lineage inference

Abstract Background: We extend algorithms for clonal lineage inference (``tumor phylogenetics'') from single-cell DNA sequence (scDNA-seq) data to accommodate broader classes of genetic variants, including single nucleotide variants (SNVs), copy number alterations (CNAs), and structural variants (SVs). Methods: We develop a computational method based on constrained optimization, posing a problem of inferring cellular lineage trees consistent with a given scDNA-seq data set constrained to follow a Dollo parsimony model for SNVs and SVs. We then seek an optimal tree consistent with these constraints so as to optimize for a CNA minimum evolution model balanced against measure of consistency of the different data types with one another relative to the reconstructed set of clones. We pose this problem as an integer linear program (ILP) that we solve heuristically via a coordinate descent algorithm. We tested the resulting method on a combination of synthetic scDNA-seq data and publicly available real data. Results: Results on synthetic data show the method to be effective at constructing lineage trees under a variety of parameter domains, including variations in noise levels, clone numbers, single cells, and mutation rates. We further show it to yield improved accuracy over widely used prior models that operate on only subsets of these variant types. Application to previously published scDNA-seq data demonstrate the method to be effective at inferring clonal lineage trees incorporating all three variant types. The results further show how the different kinds of variants can contribute in tandem to progression along single cell lineages or to the emergence of clones exhibiting hallmarks of distinct mechanisms of progression. Conclusion: The results support the effectiveness of our method in resolving accurate trees from scDNA-seq data including diverse variant types, as well as the value of considering these mutation types collectively in developing a comprehensive understanding of how various forms of somatic mutability together shape clonal evolution in cancers. Citation Format: Nishat Bristy, Xuecong Fu, Russell Schwartz. Integrating single nucleotide variants (SNVs), copy number alterations (CNAs), and structural variants (SVs) into single-cell clonal lineage inference [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2326.

Targeting oncogenic TERT promoter variants by allele-specific epigenome editing

BackgroundActivation of dominant oncogenes by small or structural genomic alterations is a common driver mechanism in many cancers. Silencing of such dominantly activated oncogenic alleles, thus, is a promising strategy to treat cancer. Recently, allele-specific epigenome editing (ASEE) has been described as a means to reduce transcription of genes in an allele-specific manner. In cancer, specificity to an oncogenic allele can be reached by either targeting directly a pathogenic single-nucleotide variant or a polymorphic single-nucleotide variant linked to the oncogenic allele. To investigate the potential of ASEE in cancer, we here explored this approach by targeting variants at the TERT promoter region. The TERT promoter region has been described as one of the most frequently mutated non-coding cancer drivers.ResultsSequencing of the TERT promoter in cancer cell lines showed 53% (41/77) to contain at least one heterozygous sequence variant allowing allele distinction. We chose the hepatoblastoma cell line Hep-G2 and the lung cancer cell line A-549 for this proof-of-principle study, as they contained two different kinds of variants, namely the activating mutation C228T in the TERT core promoter and the common SNP rs2853669 in the THOR region, respectively. These variants were targeted in an allele-specific manner using sgRNA-guided dCas9-DNMT3A-3L complexes. In both cell lines, we successfully introduced DNA methylation specifically to the on-target allele of the TERT promoter with limited background methylation on the off-target allele or an off-target locus (VEGFA), respectively. We observed a maximum CpG methylation gain of 39% and 76% on the target allele when targeting the activating mutation and the common SNP, respectively. The epigenome editing translated into reduced TERT RNA expression in Hep-G2.ConclusionsWe applied an ASEE-mediated approach to silence TERT allele specifically. Our results show that the concept of dominant oncogene inactivation by allele-specific epigenome editing can be successfully translated into cancer models. This new strategy may have important advantages in comparison with existing therapeutic approaches, e.g., targeting telomerase, especially with regard to reducing adverse side effects.

Investigating the association between BRCA1/2 copy number variation and homologous recombination deficiency score in ovarian cancer: A cross-sectional study.

e17584 Background: PARP inhibitors (PARPi) have shown significant clinical benefit as maintenance or systematic therapy in patients with ovarian cancer (OC) with BRCA1/2 mutation or positive homologous-recombination deficiency (HRD) status. However, patients with BRCA1/2 mutation not only showed better efficiency of PARPi, but also higher HRD score than other populations. Therefore, patients with BRCA1/2 mutation have received much attention. However, there are many kinds of variants in BRCA1/2 of OC patients. The purpose of this study is to explore the distribution of BRCA1/2 copy number variation (CNV) in OC patients and its association with HRD score. Methods: A cross-sectional analysis of 1636 OC patient who were retrospectively analyzed with a customized 3D-HRD panel (panel of Next-generation sequencing) between 2020 and 2022 was carried out. The HRD score was calculated as the sum of the LOH, TAI, and LST and we defined HRD score more than 30 and deleterious BRCA1/2 mutation as HRD positivity. Results: In this cohort (n = 1636), we divided the patients into 4 groups according to the BRCA1/2 status. Group1: patients with BRCA1/2 SNV (single-nucleotide variation) combined with CNV (n = 45); Group2: patient with BRCA1/2 CNV (n = 155); Group3: patient with BRCA1/2 SNV (N = 308); Group4: patient with BRCA1/2 WT (wild type, n = 1128). HRD scores decreased significantly from Group1 to Group4. And the proportion of HRD positive patients decreased significantly from Group1 to Group4. Conclusions: Different BRCA1/2 statuses lead to different HRD characterization in OC patients. OC patients with BRCA1/2 CNV (with/without BRCA1/2 SNV) showed higher HRD score than patients with BRCA1/2 SNV. These patients may deserve opportunity for PARPi treatment besides patients with germline or somatic BRCA1/2 mutation, especially for PARPi with specific requirements for patients, such as Olaparib.

A Data-Driven Lens to Understand Human Biology: An Interview with Daphne Koller

A Data-Driven Lens to Understand Human Biology: An Interview with Daphne Koller

VERIFICATION OF THE HISAB EPHEMERIS SYSTEM AGAINST THE HIJRI CALENDAR LEAP YEAR PATTERN WITH CRITERIA IMKAN AL-RUKYAH MABIMS (Case Study in Kudus District)

The hijri istilahi calendar has a 30-year cycle system, wherein 30 years there are 11 leap years and 19 basithoh years. In history, there are 4 kinds of variants in the placement of the leap year. This research aims to determine the leap year pattern of Kudus district in 30 years and to verify which patterns are close to the 4 kinds of variants. This study uses the Library Research method using a descriptive verification approach. This approach provides a sample of the number of days per month for 30 years using the Ephemeris reckoning system by considering the possibility of seeing the new moon based on the criteria of Imkan al-Rukyah MABIMS. If the hilal meets the MABIMS criteria, then the number of days is 29, but if not, then the number of days will be 30. Then, the number of days each month is accumulated annually and is used to verify the number of days each year on the hijriah istilahi calendar. Based on the analysis of the initial month data at the Kudus district headquarters for a period of 30 years, it turns out that in the period of 1411 H to 1440 H, the spread pattern of leap years is closer to pattern IV. There are 5 years whose leap is the same as the IV pattern, namely 2, 8, 16, 24, and 30.

Typen von Varianz in der Nibelungenüberlieferung

Abstract After the failure of Wilhelm Braune’s attempt to reconstruct a stemma of the Nibelungen manuscripts, traditional textual criticism lead in a dead end, even though some valuable editions (Hennig, Schulze, Reichert, Heinzle) were published. As a result of the editions of the so-called ›contaminated‹ manuscripts and a consequence of the easier access to the Nibelungen-fragments by digitalization, Nibelungen philology succeeded less and less to deal with the quantity of variants in the transmission of the text. The article proposes to distinguish three kinds of variants: First, variants due to a change in conception, a revision (for instance in the version *C). Secondly, variants based on errors in the process of transmission (by mishearing, misreading, defects of the model etc.). Only these two kinds of variants are relevant for textual criticism and for the reconstruction of a genealogy of manuscripts in the Lachmannian tradition. Thirdly, variants of lexemes, in morphology, in grammar, in syntax, which do not permit to decide between ›right‹ or ›wrong‹. It is the majority. These variants do not alter the sense of the text; they occur on all levels of transmission; the copier can use them ad libitum. They have to be excluded from textual criticism.

Role of a Rare Variant in APC Gene Promoter 1B Region in Classic Familial Adenomatous Polyposis

Background: Familial adenomatous polyposis (FAP) is most commonly caused by germline variants in the adenomatous polyposis coli (APC) gene. Although definite pathogenic variants could be detected in the majority of individuals with FAP, there are still numerous variant-negative FAP patients. Method: We utilized a 139-gene next-generation sequencing (NGS) panel and multiplex ligation-dependent probe amplification (MLPA) to detect pathogenic variants in FAP patients and found a variant-negative pedigree. Through whole-exome sequencing (WES), we identified a point variant in the noncoding region in the APC gene. Finally, we used Sanger sequencing to analyze its pedigree cosegregation and a dual-luciferase reporter (DLR) assay to assess its function. Results: With the exception of 2 variants of undetermined significance (VUS), WES showed no pathogenic or likely pathogenic variants. After performing MLPA, the pedigree was still variant-negative. Interestingly, through WES, a point variant c.-190G>A located in the promoter 1B region of the APC gene was identified in 3 affected individuals. Moreover, a variant carrier was found during screening of the family with Sanger sequencing. Through the DLR assay, we further confirmed that the variant c.-190G>A caused significant suppression of downstream transcription of APC. Conclusions: The variant (c.-190G>A) in the APC promoter 1B region is able to cause FAP with a classic phenotype, but this kind of variant in the noncoding region could be missed by conventional genetic testing. Thus, utilizing sequencing technologies covering a larger area can help us to further explore the pathogenesis in variant-negative FAP cases.

Reader expertise and the literary significance of small-scale textual features in prose fiction

Abstract We use eye tracking to investigate the attention readers pay to different textual features to determine their significance in the appreciation of prose fiction. Previous research examined attention allocation to lexical and punctuation variants, and the impact on reading dynamics for the remainder of the text, demonstrating that readers notice both kinds of variants but assign less value to the latter (Carrol, Conklin, Guy, & Scott, 2016). Here, in two experiments, we examine two conditions that may affect attention allocation: We investigate the influence of reader expertise (Experiment 1) and whether performance is influenced by a task-specific “spot-the-difference” effect (Experiment 2). We found that expertise plays little role in readers’ greater sensitivity to lexical rather than punctuation changes, and that the advantage for lexical changes persisted when the time interval between exposures is increased. These results confirm earlier findings: that small-scale features may not possess the creative significance predicated of them by critics and text-editors.

MLPA Analyses Reveal a Spectrum of Dystrophin Gene Deletions/Duplications in Pakistani Patients Suspected of Having Duchenne/Becker Muscular Dystrophy: A Retrospective Study.

Introduction: Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are inherited X-linked recessive genetic disorders caused by defects in the dystrophin gene. Abnormality in the dystrophin protein causes progressive muscle damage and weakness leading to long-term disability. Objective: To investigate the spectrum of dystrophin gene variants (deletions and duplications) in Pakistani patients suspected of having DMD/BMD or of being DMD/BMD carriers. Methods: A single center (Aga Khan University Hospital, Karachi, Pakistan) retrospective review of 46 cases was conducted to characterize dystrophin gene variants (deletion/duplication) in DMB/BMD patients using the multiplex ligation-dependent probe amplification-based method to provide coverage for all 79 exons. Results: Dystrophin gene deletions were identified in 40 of 46 cases, whereas duplications were present in 6 of 46 cases. The majority of the deletions were present between exons 45 and 52 followed by the region between exons 8 and 18. The most frequently deleted was exon 46 (8%) followed by exon 49 (7%). Dystrophin gene duplications were clustered between exons 3 and 7. The average deletion or duplication size was five exons for both kinds of variants. Conclusions: The applicability of exon skipping drugs depends on the specific mutational frequencies within populations. Our data suggest that for the Pakistani patients, multiple exon skipping between exons 46 and 49 could potentially be a target for exon skipping therapy. However, a larger nationwide study is required to further identify the predominant deletion/duplication dystrophin gene variants present in the population.

Fast-GBS: a new pipeline for the efficient and highly accurate calling of SNPs from genotyping-by-sequencing data

BackgroundNext-generation sequencing (NGS) technologies have accelerated considerably the investigation into the composition of genomes and their functions. Genotyping-by-sequencing (GBS) is a genotyping approach that makes use of NGS to rapidly and economically scan a genome. It has been shown to allow the simultaneous discovery and genotyping of thousands to millions of SNPs across a wide range of species. For most users, the main challenge in GBS is the bioinformatics analysis of the large amount of sequence information derived from sequencing GBS libraries in view of calling alleles at SNP loci. Herein we describe a new GBS bioinformatics pipeline, Fast-GBS, designed to provide highly accurate genotyping, to require modest computing resources and to offer ease of use.ResultsFast-GBS is built upon standard bioinformatics language and file formats, is capable of handling data from different sequencing platforms, is capable of detecting different kinds of variants (SNPs, MNPs, and Indels). To illustrate its performance, we called variants in three collections of samples (soybean, barley, and potato) that cover a range of different genome sizes, levels of genome complexity, and ploidy. Within these small sets of samples, we called 35 k, 32 k and 38 k SNPs for soybean, barley and potato, respectively. To assess genotype accuracy, we compared these GBS-derived SNP genotypes with independent data sets obtained from whole-genome sequencing or SNP arrays. This analysis yielded estimated accuracies of 98.7, 95.2, and 94% for soybean, barley, and potato, respectively.ConclusionsWe conclude that Fast-GBS provides a highly efficient and reliable tool for calling SNPs from GBS data.

Crystal Structure, Microstructure and Martensitic Transformation Path in Ni-Mn-In Alloys

In the present work, the crystal structure, microstructure and martensitic transformation path in Ni-Mn-In alloys were systematically studied. Results show that the austenite has a highly ordered cubic L21 structure. The martensite phase possesses a 6M incommensurate monoclinic modulated structure. The microstructure of martensite is in plate shape and self-organized in colonies. The maximum of 6 distinct martensite colonies and 24 kinds of variants in one parent grain are observed. Both of K-S and Pitsch orientation relations are found to be appropriate to describe the lattice correspondence between the parent and product phase. However, the transformation path related to Pitsch relation should be the real one that governs the transformation process in Ni-Mn-In alloys. With the determined martensitic transformation path, the formation mechanism of the microstructure of martensite phase is revealed. The 6 distinct martensite colonies are respectively generated by the six (110) planes of the cubic austenite phase during martensitic transformation. Each (110) plane transforms into four twin-related variants by changing the directions of the transformation plane and direction.

Three variants of cotton leaf curl begomoviruses with their satellite molecules are associated with cotton leaf curl disease aggravation in New Delhi

Cotton leaf curl disease (CLCuD), caused by monopartite begomoviruses and its satellite molecules, is one of the serious constrains in cultivation of cotton in India. In the present study, five CLCuD-begomovirus and its associated satellite molecules were characterized based on rolling circle amplification and sequencing of complete genome. Sequence analysis showed 82–99 % nucleotide identity among them. The phylogenetic analysis and nt identity matrix determined that of the five CLCuD-begomovirus isolates, three IARI-34, IARI-42 and IARI-50 were members of Cotton leaf curl Multan virus (CLCuMuV)-Rajasthan isolates, designated as CLCuMuV-Rajasthan-34 and two, IARI-30 and IARI-45 of Cotton leaf curl Kokhran virus (CLCuKoV)-Burewala isolates, designated as CLCuKoV-Burewala-45. The present CLCuMuV-Rajasthan-34 is recombinant isolate showing recombination events in IR, C1 and C4 regions of its genome with high probality (P = 9.9 × 10−10–3.2 × 10−6). Same species of betasatellite (1371 nt) molecules obtained from both the present isolates was related with cotton leaf curl Multan betasatellite by 89–97 % nt identity. Three alphasatellites (1366–1396 nt) related to Cotton leaf curl Burewala alphasatellite and Gossypium darwinii symptomless alphasatellite by 86 % nt identity were also obtained. This is the first report of appearance of CLCuKoV-Burewala isolate and CLCuD associated alphasatellites in New Delhi. The present study demonstrated that CLCuD in New Delhi is caused by three kinds of variants, two are strains of CLCuMuV and one of CLCuKoV, either by single or mixed infection along with beta- and alpha-satellite molecues.

Tone Quality Recognition of Instruments Based on Multi-feature Fusion of Music Signal

The traditional expert-based instrumental music evaluation strategy can’t meet the requirements of the rapidly accumulated audio data. The traditional strategy not only takes a high cost of human’s energy and time but also may have some problems on consistency and fairness of judgment. This paper aims at designing a complete recognition and evaluation strategy to automatically identify the timber of wind instruments. We take the clarinet as example and propose a strategy based on multi-feature fusion and random forest. First, we use the identification of fundamental frequency algorithm to automatically distinguish the notes performed by the instruments. Second, we extract 3 types of features including MFCC, brightness and roughness to describe the instrumental signals. Then, considering two kinds of variants: note and tone quality, we design 5 strategies to remove the influence of different notes in the evaluation of tone quality. By analyzing these strategies, we explore the optimal strategy for the recognition. The final evaluation results over 840 music slices demonstrate the effectiveness of this method.

Basic concepts and potential applications of genetics and genomics for cardiovascular and stroke clinicians: a scientific statement from the American Heart Association.

Although genetics and genomics play an increasingly large role in the practice of medicine, the clinical care of patients suffering from cardiovascular disease or stroke has not been significantly affected. This is despite the tremendous strides being made to understand the genetic basis of both rare and common cardiovascular and stroke disorders through techniques such as genome-wide association studies (GWASs) and next-generation sequencing studies. Much of this knowledge remains to be translated to the clinic and must be subjected to clinical trials to ensure patient safety and a meaningful impact on clinical outcomes. However, even if this knowledge were to be successfully implemented into clinical practice, a potential barrier to widespread adoption is a lack of familiarity with basic concepts of genetics and genomics. Another concern is the possibility of the emergence of a significant gap in clinical care provided by practitioners who are informed about the clinical use of genetics and genomics knowledge and those who are not. Thus, there is a critical need to foster genetics/genomics literacy among all involved in the care of cardiovascular and stroke patients because it can be expected that these topics will transform the way medicine is practiced. The purpose of this document is to serve as a resource for practitioners in cardiovascular and stroke medicine on the application of genetics and genomics to patient care. Although not exhaustive, it contains an overview of the field written specifically to be accessible and relevant to practitioners. It also refers to additional educational materials available in the literature, in textbooks, and on the Internet. (Because this article is intended to be primarily educational in nature, rather than providing a review of the literature, citations are limited to a small number of research articles and reviews of exceptional interest.) It recommends a core knowledge base with …

Reply to Claidière et al.: Role of psychological bias in evolution depends on the kind of culture

We showed that it is possible to produce music by a Darwinian process in which consumers select particular tunes over others (1). Our objective was to isolate the role of one element of the evolutionary process: consumer selection. In our system, heritable variation was generated by a computer algorithm. Claidiere et al. (2) argue that our methodology does not take account of the fact that the kinds of variants that humans generate are biased, and that such biases will influence the evolution of a population (e.g., ref. 3). We agree that such biases probably do …

Angioplastía de circunfleja en paciente con doble arteria descendente anterior tipo IV. Propuesta para actualizar la clasificación de Spindola-Franco

The normal anatomy of coronary arteries includes a kind of variants with regard to its origin, distribution and route, which makes that 2 patients do not have coronary arteries exactly alike. Left anterior descending artery could have anatomical variations that do not affect the normal supply of blood to the corresponding myocardial territory. In our 25 years of experience, and more than 11,000 coronary angiographies, we have found only one patient with a type IV dual left anterior descending coronary artery. In this article we show the case of a patient with the described coronary anomaly, presenting a severe stenosis of the circumflex artery which was successfully treated percutaneously. Besides, a proposal for updating the classification of Spindola-Franco is made, where the 4 types previously described were kept invariable, and 7 anatomical variants or subtypes were added.

Revising the M235T Polymorphism Position for the AGT Gene and Reporting a Modifying Variant in the Brazilian Population with Potential Cardiac and Neural Impact

There is a growing need to curate the overwhelming amount of sequencing data which is available in many public databases. For instance, new information shows that the M235T polymorphism at the angiotensinogen gene (AGT) is actually positioned at the position corresponding to the amino acid 268 and not 235. This polymorphism is filled as rs699 in the NCBI SNP database and results in the synthesis of a threonine (T) instead of a methionine (M). It has been widely studied and associated as an important risk factor for several vascular and neuropsychiatric conditions. We faced this new situation during the targeted sequencing of 360 chromosomes from Brazilian subjects studied for the M235T polymorphism, leading to the identification of a novel variation (rs141900991). This report explores the potential impact of such a dinucleotide variation, which promotes the change of alanine (A) to serine (S) at the AGT protein structure (A237S). Considering the previous M268T variation at the four possible haplotypes combined (MA, MS, TA and TS), we performed a comparative hydrophobicity simulation, using the Kyte-Doolittle algorithm, available at the CLB Bio workbench, in the four possible haplotypes. Additional simulations were performed using the programs PolyPhen, I-Mutant and SIFT, in order to evaluate the pathogenicity of both mutations. The predicted hydrophobicity decreases of a similar magnitude, with both MS and TA haplotypes, but the presence of both variations induces a major decrease in hydrophobicity, suggesting a cumulative effect, with possible modifying effect since that this variation per se would limit the hydrophobicity range and the latter chances in finding significant phenotype differences. A better characterization of this kind of variant is particularly important because the current genome wide scan analyses in complex disorders with cardiac or neural etiology are not generating reliable findings, especially if we consider the huge investment with such approach. Additional and unknown variations like this one, with potential modifying effect, might be more common than previously expected.

A class of constant modulus algorithms for uniform linear arrays with a conjugate symmetric constraint

A class of constant modulus algorithms (CMAs) subject to a conjugate symmetric constraint is proposed for blind beamforming based on the uniform linear array structure. The constraint is derived from the beamformer with an optimum output signal-to-interference-plus-noise ratio (SINR). The effect of the additional constraint is equivalent to adding a second step to the original adaptive algorithms. The proposed approach is general and can be applied to both the traditional CMA and its all kinds of variants, such as the linearly constrained CMA (LCCMA) and the least squares CMA (LSCMA) as two examples. With this constraint, the modified CMAs will always generate a weight vector in the desired form for each update and the number of adaptive variables is effectively reduced by half, leading to a much improved overall performance.