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Pegylated recombinant human granulocyte colony-stimulating factor (PEG-rhG-CSF) has been introduced for the mobilization of peripheral blood stem cells (PBSCs). However, no cases of acute lung injury (ALI) in healthy donors have been reported, and the underlying mechanisms remain poorly understood. We first reported a case of ALI caused by PEG-rhG-CSF in a healthy Chinese donor, characterized by hemoptysis, hypoxemia, and patchy shadows. Ultimately, hormone administration, planned PBSC collection, leukocyte debridement, and planned PBSC collection resulted in active control of the donor's ALI. The donor's symptoms improved without any adverse effects, and the PBSC collection proceeded without incident. Over time, the lung lesion was gradually absorbed and eventually returned to normal. PEG-rhG-CSF may contribute to ALI in healthy donors via mechanisms involving neutrophil aggregation, adhesion, and the release of inflammatory mediators in the lung. This case report examines the clinical manifestations, treatment, and mechanism of lung injury induced by PEG-rhG-CSF-mobilized PBSCs. [ABSTRACT FROM AUTHOR]

Several genes involved in the pathogenesis have been identified, with the human leukocyte antigen (HLA) system playing an essential role. However, the relationship between HLA and a cluster of hematological diseases has received little attention in China. Blood samples (n = 123913) from 43568 patients and 80345 individuals without known pathology were genotyped for HLA class I and II using sequencing-based typing. We discovered that HLA-A*11:01, B*40:01, C*01:02, DQB1*03:01, and DRB1*09:01 were prevalent in China. Furthermore, three high-frequency alleles (DQB1*03:01, DQB1*06:02, and DRB1*15:01) were found to be hazardous in malignant hematologic diseases when compared to controls. In addition, for benign hematologic disorders, 7 high-frequency risk alleles (A*01:01, B*46:01, C*01:02, DQB1*03:03, DQB1*05:02, DRB1*09:01, and DRB1*14:54) and 8 high-frequency susceptible genotypes (A*11:01-A*11:01, B*46:01-B*58:01, B*46:01-B*46:01, C*01:02-C*03:04, DQB1*03:01-DQB1*05:02, DQB1*03:03-DQB1*06:01, DRB1*09:01-DRB1*15:01, and DRB1*14:54-DRB1*15:01) were observed. To summarize, our findings indicate the association between HLA alleles/genotypes and a variety of hematological disorders, which is critical for disease surveillance. [ABSTRACT FROM AUTHOR]

Post-transplantation cyclophosphamide (PTCy) can reduce the incidence of graft versus host disease (GVHD) and this intervention is often applied on adults with hematologic malignancy. However, the high relapse rate hinders the development of the intervention and data of PTCy used on children with hematologic malignancy remains limited. In order to overcome issue of high relapse rate in PTCy treatment, we used fludarabine (Flu), enhanced dose of cytarabine (Ara-C, 9 g/m2), busulfan (Bu), Cy, anti-thymocyte globulin (ATG) combined with PTCy for an intensified conditioning regimen. A total of 22 children with acute leukemia received intensified PTCy conditioning regimen (PTCy intensified group). We matched with 18 children who received modified Bu-Cy and ATG conditioning regimen in the same period (ATG group). The two-year cumulative incidences of grade II–IV acute GVHD was significantly lower in PTCy intensified group (13.6 ± 7.7% vs 38.9 ± 11.5%, P = 0.048). Two-year GVHD-free relapse free survival (GRFS) in PTCy seems to be better among the increment group despite not being significant (63.3 ± 10.3% vs 35.4 ± 11.9%, P = 0.092). The positive rate of minimal residual disease after transplantation was significantly lower than that before transplantation (20.0% vs 2.5%, P = 0.029). In conclusion, ATG and PTCy combined with Flu-based increased intensity conditioning regimen is effective for acute leukemia in children. It could reduce GVHD rate significantly and potentially improve GRFS. [ABSTRACT FROM AUTHOR]

The function of natural killer (NK) cells has previously been implicated in hematopoietic-related diseases. Killer immunoglobulin-like receptors (KIR) play an important role in NK cells after hematopoietic stem cell transplantation. To explore the immunogenetic predisposition of hematological-related diseases, herein, a multi-center retrospective study in China was conducted, analyzing and comparing 2519 patients with hematopathy (mainly, acute lymphoblastic leukemia, acute myeloid leukemia, aplastic anemia, and myelodysplastic syndrome) to 18,108 individuals without known pathology. Genotyping was performed by polymerase chain reaction with specific sequence primers (PCR-SSP). As a result, we discovered four genes including KIR2DL5 (OR: 0.74, 95% CI 0.59–0.93; Pc = 0.0405), 2DS1 (OR: 0.74, 95% CI 0.59–0.93; Pc = 0.0405), 2DS3 (OR: 0.58, 95% CI 0.41–0.81; Pc = 0.0180), and 3DS1 (OR: 0.74, 95% CI 0.58–0.94; Pc = 0.0405) to be protective factors that significantly reduce the risk of aplastic anemia. Our findings offer new approaches to immunotherapy for hematological-related diseases. As these therapies mature, they are promising to be used alone or in combination with current treatments to help to make blood disorders a manageable disease. [ABSTRACT FROM AUTHOR]

HLA‐A*68:302 differs from HLA‐A*68:01:02:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐C*06:02:105 differs from HLA‐C*06:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐B*44:03:67 differs from HLA‐B*44:03:02:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐DPB1*05:01:18 differs from HLA‐DPB1*05:01:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐C*04:490 differs from HLA‐C*04:01:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐A*24:02:160 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐A*02:07:22 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*04:93 differs from HLA‐DQB1*04:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*03:03:29 differs from HLA‐DQB1*03:03:02:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:07:03 differs from HLA‐DRB1*14:07:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*15:644 differs from HLA‐B*15:17:01:02 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

The triallelic pattern of short tandem repeat (STR) is rare; especially, the case where this pattern exists at 4 loci has not been reported. Here, we report the type 1 triallelic patterns at D5S818, D18S51, D6S1043, and FGA from a Chinese family, which were observed during our routine chimerism assays. Before hematopoietic stem cell transplantation, the blood sample of the certain patient was analyzed by performing chimerism analysis. A preliminary STR analysis was also performed on the samples of the patient's parents. STR signal data illustrated that the sum of the peak chart areas of the two types inherited from the father was basically the same as that of the mother, belonging to the type 1 triallelic pattern. In addition, the patient's elder sister's STR result appeared to be normal. Altogether, we presented a pedigree, in which the triallelic pattern was linked by inheritance in the family. This is the first reported case of the triallelic pattern at D5S818, D18S51, D6S1043, and FGA all around the world. We hope that in the future there will be any tools to achieve accurate verification against this possibility. [ABSTRACT FROM AUTHOR]

The triallelic pattern of short tandem repeat (STR) is rare; especially, the case where this pattern exists at 4 loci has not been reported. Here, we report the type 1 triallelic patterns at D5S818, D18S51, D6S1043, and FGA from a Chinese family, which were observed during our routine chimerism assays. Before hematopoietic stem cell transplantation, the blood sample of the certain patient was analyzed by performing chimerism analysis. A preliminary STR analysis was also performed on the samples of the patient's parents. STR signal data illustrated that the sum of the peak chart areas of the two types inherited from the father was basically the same as that of the mother, belonging to the type 1 triallelic pattern. In addition, the patient's elder sister's STR result appeared to be normal. Altogether, we presented a pedigree, in which the triallelic pattern was linked by inheritance in the family. This is the first reported case of the triallelic pattern at D5S818, D18S51, D6S1043, and FGA all around the world. We hope that in the future there will be any tools to achieve accurate verification against this possibility. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:246 differs from HLA‐DRB1*14:18 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DPB1*1352:01 differs from HLA‐DPB1*02:01:02:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*15:638 differs from HLA‐B*15:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*06:02:102 differs from HLA‐C*06:02:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DPB1*02:02:07 differs from HLA‐DPB1*02:02:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

Mastering the SNP content in the HLA region can be based on it to judiciously select unrelated donor stem cells with preferable MHC matching to lower postoperative complications. Herein, quantitative PCR‐based primers and probes were designed for 10 transplants outcome‐associated SNP loci with two‐allelic polymorphism, and then a new detection system ("HLA‐10‐SNP") was established. Compared with Sanger sequencing, its accuracy has been proven to reach 100%. Additionally, fluorescent PCR typing of 10 important SNPs via this system expressed excellent repeatability (sensitivity, 20 ng). Overall, the new system achieves single‐sample classification precision and easily distinguishable results, equipped with the advantages of simple, rapid, accurate, and effective, promising to acquire widespread popularization and application in clinical settings. [ABSTRACT FROM AUTHOR]

The killer cell immunoglobulin-like receptor (KIR), which mediates the killing function of NK cells, is an attractive candidate for adoptive cellular therapy. The ethnic distribution for China provides a unique opportunity to investigate KIR gene distribution. The aim of this study was to explore the relationship between population history and the rapidly evolving KIR genetic diversity. 8050 Chinese donors from 184 hospitals were included to analyse frequency, haplotype, and B-content data of 16 KIR genes, by PCR-SSP for KIR genotyping. KIR gene carrier frequencies were found similar to those observed in other studies on Han, but different from Thais, Japanese, Africans, and populations of West Eurasian ancestry. High-frequency KIR genotype profiles found in the present population were consistent with other studies on Han populations but different from those conducted on other cohorts. The majority of our cohort carried group A KIR gene motifs. Additionally, populations with similar geographic locations in China were shown clustered together, while Hainan and Xinjiang provinces were slightly separated from these. The distribution of KIR genes varies by geographic region, and different ethnic groups may be a confounding factor of KIR diversity. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*06:475 differs from HLA‐DQB1*06:35 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*04:01:152 differs from HLA‐C*04:01:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐A*30:01:24 differs from HLA‐A*30:01:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐B*40:536N differs from HLA‐B*40:03:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐B*51:381 differs from HLA‐B*51:01:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐A*02:07:23 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:251 differs from HLA‐DRB1*14:126:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*03:621 differs from HLA‐C*03:04:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐B*13:176 differs from HLA‐B*13:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐C*12:368 differs from HLA‐C*12:03:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐C*15:02:58 differs from HLA‐C*15:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐B*35:568 differs from HLA‐B*35:03:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*48:01:11 differs from HLA‐B*48:01:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐A*24:582 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐A*24:561:02 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*12:01:12 differs from HLA‐DRB1*12:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*13:01:21 differs from HLA‐B*13:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*07:1029 differs from HLA‐C*07:02:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*06:208:02 differs from HLA‐DQB1*06:02:02 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐A*02:1075 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐A*24:02:159 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐C*01:239 differs from HLA‐C*01:02:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*55:131 differs from HLA‐B*55:02:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*03:499N differs from HLA‐DQB1*03:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*40:01:78 differs from HLA‐B*40:01:02:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]