Shenzhen Blood Center

The novel allele HLA-DQB1*03:03:31 differs from DQB1*03:03:02:02 by one synonymous nucleotide substitution in exon 2.

Hepatitis E virus (HEV)-related liver failure is increasingly reported. Patients with hyperbilirubinemia usually indicate liver damage and may develop liver failure, but HEV infection in them is less studied. This study aimed to investigate HEV infection in hyperbilirubinemia patients. A total of 949 patients with total bilirubin (Tbil) > 171 μmol/L during 2003-2021 in Beijing Youan hospital were tested for HEV. We found that 10.43% (99/949) patients were positive for anti-HEV IgM, or/and HEV pathogen markers. After ruling out 10 patients with incomplete data, 64.0% (57/89) progressed to liver failure. Patients with greater end-stage liver disease model scores tended to develop liver failure and have a poorer prognosis after HEV insult, evidenced by lower recovery/improvement rates. Liver cirrhosis patients with poorer Child-Turcotte-Pugh grades also tended to develop liver failure after HEV insult. In liver failure patients, those with HEV infection showed higher proportions of fatty liver and recent gastrointestinal haemorrhage than those without HEV infection. In conclusion, HEV infection is not uncommon in patients with Tbil > 171 μmol/L, and hyperbilirubinemia patients with more severe liver diseases are at more risk for liver failure after HEV infection.

To explore the serological characteristics and bioinformatics analysis results of 4 blood donors with RHCE*cE(281C, 282T) variant allele. A total of 4 non-related blood donors with RHCE*cE (281C, 282T) variant allele (donors 1-4) were selected as the study objects. They donated blood at Shenzhen Blood Center from January 2022 to June 2023. The 4 blood donors were all Han. And 5 mL elbow venous blood was collected from these 4 blood donors. Regular serological assaying with 4 kinds of monoclonal antibody reagents was used for determination of the RhCcEe type. The nucleotide sequences of all 10 exons and adjacent flanking intron regions of RHCE gene in these 4 donors were analyzed by Sanger sequencing, and the full-length haplotype analysis of RHCE gene was performed by using the single-molecule real-time sequencing (SMRT) third-generation technology. DeepTMHMM software was used to analyze the structure of protein transmembrane region of wild type and variant RhCcEe protein and predict the location of amino acid substitution. The effects of mutations on RhCcEe protein function were analyzed using PolyPhen-2, SIFT and Mutation Taster bioinformatics software. Robetta and Swiss-PdbViewer v4.1.0 were used for modeling the tertiary structures of RhCcEe to analyze the difference between wild type and variant RhCcEe protein. The mutation was rated according to the standards and guidelines for the classification of genetic variants of the American College of Medical Genetics and Genomics (ACMG). This study has been approved by the Medical Ethics Committee of Shenzhen Blood Center (Approval No. SZBCMEC-2022-024). The RhCcEe phenotypes of the 4 blood donors were CCEweake by serological assaying. The RhE antigen were weakly expressed form 0 to 3+. The analysis of RHCE gene sequence indicated that all the 4 donors with RHCE*cE (281C, 282T) allele. The mutation caused the substitution of a single amino acid in the RhCcEe protein (p.Leu94 Pro) and the amino acid substitution was located in the transmembrane α3 chain resulted in significant changes in the 3D structure of the extracellular region of RhCcEe protein. The substitution was predicted to be "Probably damaging", "Damaging" and "Polymorphism" by PolyPhen-2, SIFT and Mutation Taster bioinformatics software. According to the guidelines of ACMG, the variant was rated to be likely pathogenic. The RHCE*cE (281C, 282T) variant allele was first found in the Han Chinese population. The serological data of this allele were enriched. It provides an important guarantee for the safety of blood transfusion. Bioinformatics analysis provided evidences for further study of the structure and functions of RhCcEe protein.

This article presents a 100-V fly-buck converter with limited zero-current (ZC) time and implicit feedback of isolated output in the discontinuous conduction mode (DCM). An anti-noise pre-regulator is developed to resist the noise and generate stable internal supplies during high-voltage (HV) switching. AZC-time limitation scheme is designed to adjust the maximum ZC time in the DCM, such that the lowest switching frequency in the DCM is confined, and the charging frequency of the isolated outputs is guaranteed. The light-load efficiency can be improved with a lower switching frequency than working in the classical forced CCM (FCCM). Yet, the isolated output voltage seriously drops with the load in the ZC time-limited DCM, due to the loss of regulation. Therefore, an enhanced <sc xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">on</small>-time generator (EOTG) is further introduced to generate adaptive <sc xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">on</small>-time without requiring direct input or output voltage information, while realizing implicit feedback of the isolated output in the DCM. The <sc xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">on</small>-time is increased with the enlarged load of the isolated output, improving the regulation of the isolated output in the ZC-time-limited DCM. The implemented fly-buck converter prototype was fabricated in a 100-V 0.18-<inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">$\mu $</tex-math> </inline-formula>m BCD process. Up to 24% light-load efficiency improvement is achieved at <italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">VIN</i> <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">${=}\,48$</tex-math> </inline-formula>V with a 25-<inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> <tex-math notation="LaTeX">$\mu $</tex-math> </inline-formula>s ZC time limitation. The measured peak efficiency is 94.4% with a 24-V input voltage.

Cervical cytology is a critical screening strategy for early detection of pre-cancerous and cancerous cervical lesions. The challenge lies in accurately classifying various cervical cytology cell types. Existing automated cervical cytology methods are primarily trained on databases covering a narrow range of coarse-grained cell types, which fail to provide a comprehensive and detailed performance analysis that accurately represents real-world cytopathology conditions. To overcome these limitations, we introduce HiCervix, the most extensive, multi-center cervical cytology dataset currently available to the public. HiCervix includes 40,229 cervical cells from 4,496 whole slide images, categorized into 29 annotated classes. These classes are organized within a three-level hierarchical tree to capture fine-grained subtype information. To exploit the semantic correlation inherent in this hierarchical tree, we propose HierSwin, a hierarchical vision transformer-based classification network. HierSwin serves as a benchmark for detailed feature learning in both coarse-level and fine-level cervical cancer classification tasks. In our comprehensive experiments, HierSwin demonstrated remarkable performance, achieving 92.08% accuracy for coarse-level classification and 82.93% accuracy averaged across all three levels. When compared to board-certified cytopathologists, HierSwin achieved high classification performance (0.8293 versus 0.7359 averaged accuracy), highlighting its potential for clinical applications. This newly released HiCervix dataset, along with our benchmark HierSwin method, is poised to make a substantial impact on the advancement of deep learning algorithms for rapid cervical cancer screening and greatly improve cancer prevention and patient outcomes in real-world clinical settings.

MICB*002:06 differs from MICB*002:01:01 by one nucleotide change at nucleotide 33 in exon 1 from C to T.

Identifying host factors involved in maintaining human immunodeficiency virus type 1 (HIV-1) latency and understanding their mechanisms prepares the groundwork to discover novel targets for HIV-1 latent infection and provides further options for the selection of latency-reversing agents in the "shock" strategy. In this study, we identified a novel role of the DNA replication factor origin recognition complex 1 (ORC1) in maintaining repressive chromatin structures surrounding the HIV-1 promoter region, thereby contributing to HIV-1 latency. This discovery expands our understanding of the non-replicative functions of the ORC complex and provides a potential therapeutic strategy for HIV-1 cure.

One nucleotide substitution in codon 30 of HLA-DRB4*01:03:01:01 results in a novel allele, HLA-DRB4*01:179.