Genomic full-length sequence of the HLA-B*13:64 allele was identified in a Chinese bone marrow donor.

Genomic full-length sequence of HLA-B*13:64 was identified in a Chinese individual by sequence-based typing.

A novel HLA-C*07 allele, HLA-C*07:1024, was identified in a Chinese individual.

One nucleotide replacement at nucleotide 397 of HLA-C*07:02:01:01 results in a new allele, HLA-C*07:1024.

Identification of the novel HLA-C*14:02:38 allele in a Chinese individual.

HLA-C*14:02:38 differs from HLA-C*14:02:01:01 by one nucleotide at position 288 in exon 2.

Genomic full-length sequence of the HLA-A*11:264 allele was identified in a Chinese bone marrow donor.

Genomic full-length sequence of HLA-A*11:264 was identified in a Chinese individual by sequence-based typing.

Identification of the novel HLA-A*02:406 allele in a Chinese individual.

HLA-A*02:406 was initially identified in a volunteer donor for China Marrow Donor Program.

Genomic full-length sequence of the HLA-B*44:127 allele was identified in a Chinese bone marrow donor.

Genomic full-length sequence of HLA-B*44:127 was identified in a Chinese individual by sequence-based typing.

A novel HLA-A*33 allele, HLA-A*33:131, identified by sequencing-based typing.

The novel allele HLA-A*33:131 was identified in a Chinese individual using the sequencing-based typing method.

Identification of a novel HLA-B*40 allele, B*40:01:43, in a Chinese individual.

HLA-B*40:01:43 was initially identified in a volunteer donor for China marrow donor program by sequence-based typing.

[Sequence Analysis of A Novel HLA-B*13:68 Allele].

OBJECTIVE: The purpose of this research was to identify a novel HLA-B allele in Chinese population. METHODS: The HLA typing of bone marrow donors was performed by PCR-SBT. The ambiguous novel HLA allele was confirmed with GSSP method. RESULTS: The sequence of a sample was different from all alleles in the HLA-B databases. The sequence analysis showed that it differed from the closet matching allele HLA-B*13:01:01 at one nucleotide substitution, 137 T > C in Exon2, which resulted in an amino acid change from Phenylalanine (Phe) to Serine (Ser) at codon 22. CONCLUSION: A novel allele was identified and named as HLA-B*13:68 by the WHO Nomenclature Committee.

[Sequencing analysis and identification of a novel HLA-B(*)40:162 allele].

The aim of this study was to identify a novel HLA-B allele in Chinese population. The HLA typing of bone marrow donors was performed by PCR-SBT. The ambiguous novel HLA allele was confirmed with GSSP and single stranded SBT method. The result indicated that there was a sample, the sequence of which was different from all alleles in the HLA databases. The sequence analysis showed that it differed from the closet matching allele B(*)40:06:01 in one nucleotide substitution, 272 C>T in Exon 2, which resulted in an amino acid change from Serine (Ser) to Phenylalanine (Phe) at codon 63. It is concluded that the novel allele has been identified and is named HLA-B(*)40:162 by the WHO Nomenclature Committee.

Trehalose inhibited the phagocytosis of refrigerated platelets in vitro via preventing apoptosis.

BACKGROUND: The sole reason that platelets (PLTs) are currently stored at room temperature is that refrigeration of PLTs results in their rapid clearance after transfusion. Recent data have suggested that trehalose was an effective cryoprotective reagent for human PLTs. This study evaluated the effect of trehalose on the phagocytosis of refrigerated PLTs. STUDY DESIGN AND METHODS: Phagocytosis of PLTs was evaluated with THP-1 cells. Phosphatidylserine exposure and caspase-3 activity in PLTs were measured with flow cytometry. PLT mitochondrial transmembrane potentials were studied by staining PLTs with JC-1. Expression of Bcl-XL and Bax was determined by Western blot. PLT aggregation was studied in vitro with a PLT aggregation profiler. RESULTS: It was demonstrated that trehalose significantly inhibited the phagocytosis of refrigerated PLTs by showing that the phagocytotic ratio of PLTs refrigerated with trehalose for 9 days was generally comparable with that of PLTs stored at room temperature for 5 days, which was significantly lower than that of PLTs refrigerated without trehalose. Further studies revealed that trehalose could prevent the apoptosis of refrigerated PLTs, which was determined by the phosphatidylserine exposure, caspase-3 activities, mitochondrial transmembrane potentials, and expression of Bcl-XL and Bax. Finally, it was shown that PLTs refrigerated with trehalose for 9 days also maintained their activity to aggregate when exposed to agonists in a standard aggregometry assay. CONCLUSION: Our results suggest that trehalose could inhibit the phagocytosis of refrigerated PLTs in vitro through preventing apoptosis, implying that trehalose is a promising candidate to optimize the refrigeration of human PLTs.