Biomedical subjects

Wenwei Chen

Publications and source records attributed to Wenwei Chen.

6 recordsLinked to original sources

PubMed2026

Interface Excitons in van der Waals Sandwich Heterostructures.

Exciton engineering in van der Waals heterostructures (vdWHs) is essential for next-generation optoelectronics, yet they normally require near-perfect stacking and are highly sensitive to moiré potentials. Here, we demonstrate a polarity-engineering strategy using a γ-InSe/transition metal dichalcogenide/γ-InSe sandwich heterostructure. The out-of-plane spontaneous polarization of γ-InSe intrinsically breaks interfacial inversion symmetry, giving rise to interface excitons (IFXs) that exhibit a linear Stark effect with an ultrasmall dipole moment of 0.15 e·nm. First-principles calculations and Kelvin probe force microscopy reveal asymmetric interfacial charge transfer governed by γ-InSe's polarity. Transient spectroscopy shows nonmonotonic relaxation dynamics, including a characteristic signal reversal that indicates pre-existing interfacial charge states. Our results establish that exciton dipole moments, interlayer coupling, and relaxation dynamics can be precisely tuned through material polarity and thickness. Polarity engineering thus provides a versatile and robust route to control excitonic properties in vdWHs, offering expanded design strategies for advanced excitonic and optoelectronic devices.

Stark effect↗

PubMed2006

Global variation in copy number in the human genome.

Copy number variation (CNV) of DNA sequences is functionally significant but has yet to be fully ascertained. We have constructed a first-generation CNV map of the human genome through the study of 270 individuals from four populations with ancestry in Europe, Africa or Asia (the HapMap collection). DNA from these individuals was screened for CNV using two complementary technologies: single-nucleotide polymorphism (SNP) genotyping arrays, and clone-based comparative genomic hybridization. A total of 1,447 copy number variable regions (CNVRs), which can encompass overlapping or adjacent gains or losses, covering 360 megabases (12% of the genome) were identified in these populations. These CNVRs contained hundreds of genes, disease loci, functional elements and segmental duplications. Notably, the CNVRs encompassed more nucleotide content per genome than SNPs, underscoring the importance of CNV in genetic diversity and evolution. The data obtained delineate linkage disequilibrium patterns for many CNVs, and reveal marked variation in copy number among populations. We also demonstrate the utility of this resource for genetic disease studies.

Chromosome Mapping↗

PubMed2006

Genome-wide detection of human copy number variations using high-density DNA oligonucleotide arrays.

Recent reports indicate that copy number variations (CNVs) within the human genome contribute to nucleotide diversity to a larger extent than single nucleotide polymorphisms (SNPs). In addition, the contribution of CNVs to human disease susceptibility may be greater than previously expected, although a complete understanding of the phenotypic consequences of CNVs is incomplete. We have recently reported a comprehensive view of CNVs among 270 HapMap samples using high-density SNP genotyping arrays and BAC array CGH. In this report, we describe a novel algorithm using Affymetrix GeneChip Human Mapping 500K Early Access (500K EA) arrays that identified 1203 CNVs ranging in size from 960 bp to 3.4 Mb. The algorithm consists of three steps: (1) Intensity pre-processing to improve the resolution between pairwise comparisons by directly estimating the allele-specific affinity as well as to reduce signal noise by incorporating probe and target sequence characteristics via an improved version of the Genomic Imbalance Map (GIM) algorithm; (2) CNV extraction using an adapted SW-ARRAY procedure to automatically and robustly detect candidate CNV regions; and (3) copy number inference in which all pairwise comparisons are summarized to more precisely define CNV boundaries and accurately estimate CNV copy number. Independent testing of a subset of CNVs by quantitative PCR and mass spectrometry demonstrated a >90% verification rate. The use of high-resolution oligonucleotide arrays relative to other methods may allow more precise boundary information to be extracted, thereby enabling a more accurate analysis of the relationship between CNVs and other genomic features.

Algorithms↗

PubMed2005

Can an allograft become harmonious with its recipient by analogous mechanisms to the long-term survival of a parasite in its host? Transplantation is similar to parasitism and chronic parasite infection can prolong allograft survival.

Organ transplantation is very similar to the parasitism, the immune responses to the allograft and parasite share some general characters in acute stage. But host-parasite interplay seems harmonious and clinically asymptomatic carriers act as long-term reservoirs for transmission even several decades. It is proposed that the allograft also can survive long-term like the parasite harmonious with the host if we exploit the mechanism of the parasitism. How can the parasite escape the immunologic cleaning? Recent research found that: (1) Almost all the parasites infection can break the balance of Th1/Th2 and induce the Th2 bias. The level of cytokine excreted by Th2 is increased. (2) Parasite infection can interfere in antigen presentation processing through cystatins and "dendritic cell paralysis". (3) Regulatory T cells were found surrounding the local site of parasite worms. (4) Parasite infections can switch of eicosanoid metabolism, and the anti-inflammatory mediator of the plasma is increasingly manifest in the chronic infection stage. And in animal model, chronic infection can prolong the allograft survival. If the hypotheses are correct, it will give another novel therapeutic option for patients with organ transplantation.

Chronic Disease↗

PubMed2004

Whole-genome scan, in a complex disease, using 11,245 single-nucleotide polymorphisms: comparison with microsatellites.

Despite the theoretical evidence of the utility of single-nucleotide polymorphisms (SNPs) for linkage analysis, no whole-genome scans of a complex disease have yet been published to directly compare SNPs with microsatellites. Here, we describe a whole-genome screen of 157 families with multiple cases of rheumatoid arthritis (RA), performed using 11,245 genomewide SNPs. The results were compared with those from a 10-cM microsatellite scan in the same cohort. The SNP analysis detected HLA*DRB1, the major RA susceptibility locus (P=.00004), with a linkage interval of 31 cM, compared with a 50-cM linkage interval detected by the microsatellite scan. In addition, four loci were detected at a nominal significance level (P<.05) in the SNP linkage analysis; these were not observed in the microsatellite scan. We demonstrate that variation in information content was the main factor contributing to observed differences in the two scans, with the SNPs providing significantly higher information content than the microsatellites. Reducing the number of SNPs in the marker set to 3,300 (1-cM spacing) caused several loci to drop below nominal significance levels, suggesting that decreases in information content can have significant effects on linkage results. In contrast, differences in maps employed in the analysis, the low detectable rate of genotyping error, and the presence of moderate linkage disequilibrium between markers did not significantly affect the results. We have demonstrated the utility of a dense SNP map for performing linkage analysis in a late-age-at-onset disease, where DNA from parents is not always available. The high SNP density allows loci to be defined more precisely and provides a partial scaffold for association studies, substantially reducing the resource requirement for gene-mapping studies.

Arthritis, Rheumatoid↗

PubMed2003

Large-scale genotyping of complex DNA.

Genetic studies aimed at understanding the molecular basis of complex human phenotypes require the genotyping of many thousands of single-nucleotide polymorphisms (SNPs) across large numbers of individuals. Public efforts have so far identified over two million common human SNPs; however, the scoring of these SNPs is labor-intensive and requires a substantial amount of automation. Here we describe a simple but effective approach, termed whole-genome sampling analysis (WGSA), for genotyping thousands of SNPs simultaneously in a complex DNA sample without locus-specific primers or automation. Our method amplifies highly reproducible fractions of the genome across multiple DNA samples and calls genotypes at >99% accuracy. We rapidly genotyped 14,548 SNPs in three different human populations and identified a subset of them with significant allele frequency differences between groups. We also determined the ancestral allele for 8,386 SNPs by genotyping chimpanzee and gorilla DNA. WGSA is highly scaleable and enables the creation of ultrahigh density SNP maps for use in genetic studies.

Algorithms↗