Institute of Transfusion Medicine

Beijing, China

Institute of Transfusion Medicine

Beijing, China
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Zhang X.,Uppsala University | Wang B.,Uppsala University | Wang B.,Beijing Institute of Pharmacology and Toxicology | O'Callaghan P.,Uppsala University | And 11 more authors.
Acta Neuropathologica | Year: 2012

Neuroinflammation is typically observed in neurodegenerative diseases such as Alzheimer's disease, as well as after traumatic injury and pathogen infection. Resident immune cells, microglia and astrocytes, are activated and joined by blood-borne monocytes that traverse the blood-brain barrier and convert into activated macrophages. The activated cells express various cytokines, chemokines and proteolytic enzymes. To study the role of heparan sulfate proteoglycans in neuroinflammation, we employed a transgenic mouse overexpressing heparanase, an endoglucuronidase that specifically degrades heparan sulfate side chains. Neuroinflammation was induced by systemic challenge with lipopolysaccharide, or by localized cerebral microinjection of aggregated amyloid-β peptide, implicated in Alzheimer's disease. Lipopolysaccharide- treated control mice showed massive activation of resident microglia as well as recruitment of monocyte-derived macrophages into the brain parenchyma. Microinjection of aggregated amyloid- β elicited a similar inflammatory response, albeit restricted to the injection site, which led to dispersion and clearance of the amyloid. In the heparanase-overexpressing mice, all aspects of immune cell recruitment and activation were significantly attenuated in both inflammation models, as was amyloid dispersion. Accordingly, an in vitro blood- brain barrier model constructed from heparanase-overexpressing cerebral vascular cells showed impaired transmigration of monocytes compared to a corresponding assembly of control cells. Our data indicate that intact heparan sulfate chains are required at multiple sites to mediate neuroinflammatory responses, and further point to heparanase as a modulator of this process, with potential implications for Alzheimer's disease. © Springer-Verlag 2012.

Ziemann M.,Institute of Transfusion Medicine | Juhl D.,Institute of Transfusion Medicine | Brockmann C.,Institute of Transfusion Medicine | Gorg S.,Institute of Transfusion Medicine | Hennig H.,Institute of Transfusion Medicine
Transfusion | Year: 2017

BACKGROUND: DNA of human cytomegalovirus (CMV) is frequently detected in plasma of donors with primary CMV infection. It is unknown, however, whether leukoreduced blood products from these donors contain sufficient amounts of infectious virus to cause transfusion-transmitted CMV infections (TT-CMV). STUDY DESIGN AND METHODS: During a 14-year period, CMV DNA-positive donations were identified as part of several previously published studies. Additionally, further donors with seroconversion were tested for CMV DNA. The serostatus of patients who had received a CMV DNA-positive blood product was determined out of pretransfusion samples. Later samples were examined for development of CMV antibodies. Patients with a follow-up of less than 140 days were also tested for CMV DNA. RESULTS: A total of 221 blood products from CMV DNA-positive donations were transfused to 219 recipients. Pretransfusion samples were available for 179 patients, of whom 62 (34.6%) were seronegative. For 39 seronegative recipients of 40 blood products follow-up samples drawn at least 30 days after transfusion were available. The median duration of follow-up was 287 days (range, 38-3784 days). Thirty-six patients were still CMV seronegative in their last sample. Three patients were CMV seropositive due to passive antibody transfer by plasma rich products from seropositive donors, but CMV DNA negative in all tested samples. CONCLUSION: TT-CMV was excluded in all recipients of 40 blood products from CMV DNA-positive donations. This corresponds to a 95% interval of confidence for the risk of TT-CMV of less than 7.4%. Because no patient belonged to a typical at-risk population, the results are only valid for immunocompetent subjects. © 2017 AABB.

Makarovska-Bojadzieva T.,Institute of Transfusion Medicine | Velkova E.,Institute of Transfusion Medicine | Blagoevska M.,Institute of Transfusion Medicine
Macedonian Journal of Medical Sciences | Year: 2017

BACKGROUND: Red blood cell (RBC) alloimmunization is still an actual problem in our transfusion practice. In 2011, in addition to the regular ABO/D blood group typing, phenotyping for Rh (C, c, E, e) and Kell antigens was introduced for blood donors and patients undergoing blood transfusion. Our aim was to evaluate the impact of the extended RBC typing and donor/recipient matching on the incidence of RBC alloimmunization. METHODS: A retrospective comparative study was conducted by reviewing RBC request records for about 36,000 patients transfused with RBC in the period from 2013 to 2015 in comparison to the similar study conducted on 47,000 transfused patients in the period from 2005 to 2008. Pre-transfusion serologic testing data were retrieved for analysis. Blood samples with positive antibody screening and positive cross-match were further subjected to antibody identification. All the tests were performed using column agglutination technique (CAT) with ID-cards and reagents from DiaMed in both studies. RESULTS: Irregular RBC alloantibodies were detected in 116 (0.32%) out of 36,000 transfused patients. Multiple transfusions (15.8 units/patient) were given to 450 patients from which 79 (17.5%) had RBC allontibodies. The incidence of RBC alloimmunisation in the rest of the 35,550 transfused patients from which 37 had RBC alloantibodies was 0.10%. A total of 117 alloantibodies were identified in 96 out of the 116 patients with irregular RBC antibodies. Their specificity was as fallows: anti-E (25.6%), -C (6.0%), -c (8.5%), -e (0.85%), -Cw (5.1%), -K (12.8%), -Fya (10.2%), -Fyb (2.5%), -Jka (7.7%), - Jkb (2.5%), -M (9.4%), -S (1.7%), -s (0.85%), -Lua (1.7%), -Leb (3.4%) and anti- Leb (0.85%). Multiple antibodies were identified in 22 of the transfused patients out of which 15 (68.2%) received multiple transfusions. Anti-E was the most common antibody found in more of the 50% of the multiple antibody cases. CONCLUSIONS: The overall incidence of RBC alloimmunization in transfused patients decreased from 0.51% which was the estimated incidence for the period before the introduction of the extended RBC typing (2005-2008) to 0.32% (2013-2015). This is due to the decreased incidence of RBC alloimmunization in the multiply transfused patients from 33.9% to 17.5% respectively. The current frequency of anti-E (25.6%) and -K (12.8%) antibodies in transfused patients are significantly lower than their previous estimated frequencies of 30.4% and 24.0% respectively, as well as the overall frequency of RBC antibodies to Rh+Kell antigens which decreased from 72.4% to 53.8%. Extended donor-recipient matching for C, c, E, e and Kell antigens has proved a beneficial effect on the incidence of RBC alloimmunization in multiply transfused patients. © 2017 Tatjana Makarovska-Bojadzieva, Emilija Velkova, Milenka Blagoevska.

Han B.,Institute of Transfusion Medicine
Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics | Year: 2017

OBJECTIVE: To determine the genotypes of three blood samples suspected as B subtype through DNA sequencing.METHODS: The samples were first genotyped with PCR-SSP. Exons 6 and 7 of the ABO genes were subjected to PCR, direct sequencing, and cloned sequencing to determine the genotypes.RESULTS: Serological results of the three samples were similar, with red cells being weakly agglutinatable by anti-B and serum containing anti-B. The samples were preliminarily genotyped as B/O1. Sequencing analysis showed that all three samples contained an O allele and a 905A>G mutation of the B gene, which was previously defined as Bx02.CONCLUSION: Through sequencing analysis, the three samples typed as B subtype with serological testing were identified as Bx phenotype. The genotype of samples 1 and 2 was Bx02/O101, and that of sample 3 was Bx02/O102.

Ma K.R.,Institute of Transfusion Medicine
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2011

This study was purposed to investigate the molecular basis of a para-Bombay phenotype for screening and identification of rare blood group. ABO and H phenotypes of the proband were identified by serological techniques. The exon 6 to exon 7 of ABO gene and full coding region of α-1,2-fucosyltransferase (fut1) gene of the proband were analyzed by polymerase chain reaction and direct sequencing of the amplified fragments. The haplotype of compound heterozygote of fut1 was also identified by cloning sequencing. The results indicated that a rare para-Bombay phenotype was confirmed by serological techniques. Two deletion or insertion variant sites near nucleotide 547 and 880 were detected in fut1 gene. The results of cloning sequence showed that one haplotype of fut1 gene was two bases deletion at 547-552 (AGAGAG→AGAG), and another one was two bases deletion at position 880-882 (TTT→T). Both two variants caused a reading frame shift and a premature stop codon. It is concluded that a rare para-Bombay phenotype is found and confirmed in blood donor population. The molecular basis of this individual is compound heterozygote of two bases deletion on fut1 gene which weaken the activity of α-1, 2-fucosyltransferase.

Yin H.-Q.,Institute of Transfusion Medicine | Xiao R.,Beijing Institute of Radiation Medicine | Rong Z.,Beijing Institute of Radiation Medicine | Jin P.-P.,Institute of Transfusion Medicine | And 2 more authors.
Methods | Year: 2015

The evanescent wave fiber immunosensors (EWFI) technique was developed for the real-time rapidly sensitive and specific detection of the monoclonal antibody 3E2 of BTV. The outer-core protein VP7 of BTV was labled on the surface of the exposed fiber-optic core. The monoclonal antibody 3E2 of BTV VP7 were added and then the goat ant-rat IgG conjugated with Cy3 was captured. After the 532. nm pulse (excitation source) reached the fiber probe, evanescent wave was generated, which excited the Cy3 bound to the immuno-complex and produced the fluorescent signal, which was changed into electrical signals read through computer. The preliminary results suggested that a detection limit of 10. ng/ml was measured for the monoclonal antibody 3E2, which is equal to the sensitivity of ELISA. The 3E2 sample was specifically detected through the EWFI assay in 15. min, and the fiber can be recycled at least ten times through TEA solution condition. This developed EWFI was a real-time rapidly sensitive and specific way for the detection of BTV antibodies. © 2015.

Hiemann N.E.,Deutsches Herzzentrum Berlin | Meyer R.,Deutsches Herzzentrum Berlin | Wellnhofer E.,Deutsches Herzzentrum Berlin | Schoenemann C.,Institute of Transfusion Medicine | And 4 more authors.
Transplantation | Year: 2012

BACKGROUND: Non-human leukocyte antigen antibodies (Abs) targeting vascular receptors are implicated in the pathogenesis of renal allograft vascular rejection and in progressive vasculopathy in patients with systemic sclerosis. METHODS: We prospectively tested in 30 heart transplant recipients the impact of Abs directed against endothelin-1 type A (ETAR) and angiotensin II type 1 receptors (AT1R, cell-enzyme-linked immunosorbent assay) at time of transplantation and during the first posttransplantation year on cellular and Ab-mediated rejection (immunohistochemistry, C3d, and immunoglobulins) and microvasculopathy in endomyocardial biopsy. RESULTS: Cellular rejection, Ab-mediated rejection, and microvasculopathy was found in 40% and 13%, 57% and 18%, and 37% and 40% of biopsies at 1 month and 1 year posttransplantation, respectively. Maximum levels of AT1R and ETAR Abs were higher in patients with cellular (16.5±2.6 vs. 9.4±1.3; P=0.021 and 16.5±2.5 vs. 9.9±1.9; P=0.041) and Ab-mediated rejection (19.0±2.6 vs. 10.0±1.3; P=0.004 and 19.4±2.7 vs. 9.0±1.7; P=0.002), as compared with patients who had no rejection. Patients with elevated AT1R Abs (53% [16/30]) or ETAR Abs (50% [15/30]; pretransplantation prognostic rejection cutoff >16.5 U/L) presented more often with microvasculopathy (both, 67% vs. 23%; P=0.048) than patients without. CONCLUSIONS: Elevated levels of AT1R and ETAR Abs are associated with cellular and Ab-mediated rejection and early onset of microvasculopathy and should be routinely monitored after heart transplantation. © 2012 by Lippincott Williams & Wilkins.

Lu H.J.,Institute of Transfusion Medicine
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2012

This study was aimed to discriminate the alleles in the HLA-C*07:01:01G and HLA-C*07:02:01G groups and analyze their associations with HLA-B locus. Samples previously typed as HLA-C*07:01:01G and HLA-C*07:02:01G were collected. The nucleotide sequences in exons 1 to 7 of the HLA-C locus were sequenced by polymerase chain reaction sequence-based typing (PCR-SBT) and HLA-B genotyping was also preformed by PCR-SBT in these samples. The results showed that 4 samples (30.8%) were confirmed as HLA-C*07:01:01 and 9 samples (69.2%) were HLA-C*07:06 among 13 samples previously typed as HLA-C*07:01:01G. Linkage disequilibrium (LD) analysis showed that HLA-C*07:06 allele was strongly related with HLA-B*44:03. All samples were typed as C*07:02:01 among 102 individuals previously typed as C*07:02:01G. LD analysis showed that C*07:02:01 was strongly related with HLA-B*51:01, B*46:01, B*39:01, B*40:01, B*38:02, B*15:02 alleles. It is concluded that HLA-C*07:01:01 and HLA-C*07:06 alleles are confirmed in the HLA-C*07:01:01G group and HLA-C*07:02:01 is a preferred allele in the HLA-C*07:02:01G.

Parkner A.M.,Institute of Transfusion Medicine | Halm-Heinrich I.,Institute of Transfusion Medicine | Hahn J.,Institute of Transfusion Medicine | Heim M.U.,Institute of Transfusion Medicine
Tissue Antigens | Year: 2012

The newly detected HLA-B*15:238 is distinguished from HLA-B*15:52 by a single-nucleotide exchange at position 527 where T is replaced by A. © 2012 John Wiley & Sons A/S.

Liu Y.,Institute of Transfusion Medicine
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2013

The individual with the deficiency of CD36 antigen on platelet displayed the risk of anti-CD36 immune reaction induced by transfusion, which is one of the reasons for platelet transfusion refractoriness (PTR). This study was purposed to detect the expression level of CD36 antigen on platelet by flow cytometry among apheresis platelet donors of Hangzhou area, and the frequency of CD36 deficiency was analyzed. Platelet-rich plasma (PRP) was separated from fresh anticoagulant whole blood by centrifugation, then the platelets were washed and adjusted to 1×10(6). The platelets were incubated with FITC-labeled CD36 and PE-labeled CD41 monoclonal antibodies, then the expression level of CD36 was detected by flow cytometry. The CD36 expression on monocytes for the samples of CD36-deficiency on the platelets was further analyzed. The results showed that 7 samples with CD36 antigen deficiency were found in 192 apheresis platelet donors. The frequency of CD36 deficiency was 3.6% and all of them were typeII deficiency. The significant difference of CD36 antigen expression was observed in the platelet donors of Hangzhou population, among them 59 individuals with low expressed CD36 antigen and 126 individuals with highly expressed CD36 antigen were found according to the geometric mean fluorescence intensity. It is concluded that the CD36 antigen deficient phenotype existed in the population, these data will provide the information for research of the CD36 antigen distribution and help to solve the platelet transfusion refractoriness.

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