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Journal articles on the topic "(donor) (copy 2)"
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Goncharova, Anna S., Evgeniy N. Kolesnikov, Ekaterina V. Zaikina, A. V. Volkova, M. V. Mindar, D. V. Khodakova, Ekaterina A. Lukbanova, et al. "Correlation of SOX-2 and NOTCH1 copy numbers with vimentin expression in orthotopic patient-derived xenografts of cardioesophageal cancer in immunodeficient mice." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e15034-e15034. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15034.
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e15034 Background: Cardioesophageal cancer is one of the most common tumors affecting the mucosa of the cardiac stomach and distal esophagus. Despite the variety of treatment strategies and chemotherapy agents, the prognosis for the patients remains poor. The purpose of the study was to analyze the relative copy numbers of SOX-2 and NOTCH1 and vimentin expression in orthotopic patient-derived xenografts of cardioesophageal cancer. Methods: The model of cardioesophageal cancer was created in Balb/c Nude mice with surgical bioptates of moderately differentiated adenocarcinoma obtained from a donor with infiltrative ulcerative cancer of the lower third of the esophagus with a transition to the cardiac stomach into the distal esophagus of Balb/c Nude mice. The index of proliferative activity in the bioptates was assessed by IHC. The relative copy numbers of SOX-2 and NOTCH1 and vimentin expression were determined by Real-Time qPCR. Results: Expression of vimentin was absent in tissues of the donor tumor. The levels of vimentin expression statistically significantly increased in xenografts (1+ and 3+). The SOX-2 and NOTCH1 relative copy numbers were statistically significantly increased in tissues of the donor tumor (0.9 and 0.7), compared to xenografts (1.5±0.03 and 1.7±0.03). Molecular genetic analysis demonstrated an association between an increased vimentin expression and changes in the relative copy numbers of SOX-2 and NOTCH1 (p = 0.013 and p = 0.0001). Conclusions: The relative copy numbers of SOX-2 and NOTCH1 genetic loci was associated with increased expression of the epithelial-mesenchymal transition marker vimentin in tumor tissue samples and changed with each new generation of orthotopic xenografts.
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Ghassemzadeh, Mitra, Klaus Harms, Kurt Dehnicke, and Jörg Magull. "μ2-Chlorokomplexe von Succinimid und N-Chlorsuccinimid. Die Kristallstrukturen von PPh4[Cl(Succinimid)2], PPh4[[Cl(N-Cl-Succinimid)2] und N-Chlorphthalimid / μ2-Chloro Complexes of Succinimide and N-Chlorosuccinimide. The Crystal Structures of PPh4[Cl(Succinimide)2], PPh4[Cl(N-Cl-Succinimide)2] and N-Chlorophthalimide." Zeitschrift für Naturforschung B 49, no. 4 (April 1, 1994): 506–12. http://dx.doi.org/10.1515/znb-1994-0413.
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Abstract The donor-acceptor complexes PPh4[Cl(succinimide)2] and PPh4[Cl(N-chlorosuccinimide)2] have been prepared by reactions of PPh4Cl with succinimide and N-chlorosuccinimide, re spectively. in acetonitrile solutions. The complexes have been characterized by IR spectros copy and by crystal structure determinations. The crystal structure of N-chlorophthalimide has also been solved.
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Kaneda, M., S. Watanabe, Y. Hirao, S. Akagi, S. Haraguchi, T. Somfai, K. Takeda, M. Hirako, M. Geshi, and T. Nagai. "47 DIFFERENCES IN MITOCHONDRIAL DNA COPY NUMBER AND EPIGENETIC PATTERNS OF MITOCHONDRIA-RELATED GENES IN CLONED COWS FROM THE SAME DONOR CELLS." Reproduction, Fertility and Development 25, no. 1 (2013): 171. http://dx.doi.org/10.1071/rdv25n1ab47.
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The genetic codes of cloned animals and the donor are identical; however, incomplete reprogramming of donor nuclei during NT causes epigenetic abnormalities in cloned animals. Due to the genetic identity and epigenetic differences among clones, we can study epigenetic effects on the phenotypes by analyzing genetically identical clones. During the NT process, donor cell mitochondria (mt) are transferred into the recipient oocytes and mtDNA heteroplasmy is observed. Previous studies have reported various mtDNA transmission patterns not only in the cloned animal itself but also in the offspring of clones. However, differences in mtDNA copy number in cloned animals have not been reported, especially genetically identical ones. To analyze the genetic effects on mtDNA copy number in cattle, we compared actual mtDNA copy number per diploid genome in various tissues of clones derived from the same donor cells. From 5 genetically identical cloned cows (Japanese Black cattle, ages 68 to 82 months) and 6 non-cloned cows (Japanese Black cattle, ages 52 to 129 months), we isolated DNA from 8 kinds of tissues (heart, lung, liver, kidney, spleen, small intestine, muscle, and spinal cord) and measured mtDNA copy number by using real-time PCR. The absolute copy numbers of 2 mtDNA-encoded genes (COX1 and CytB) and 2 nuclear-encoded genes (H19 and IGF2) were measured and analyzed. To examine the epigenetic effects on mitochondria-related genes, we also analyzed DNA methylation patterns of mitochondria-related gene ANT4 (mitochondrial ADP-ATP translocase) in these tissues by the combined bisulfite restriction analysis (COBRA) method. The actual mtDNA copy number per diploid genome varied in tissues and individuals both in clones and non-clones (average in clones v. non-clones: heart: 11 839 ± 6210 v. 9569 ± 2555; lung: 2027 ± 1153 v. 1383 ± 173; liver: 5644 ± 2278 v. 4799 ± 1848; spleen: 1080 ± 844 v. 393 ± 265; kidney: 7034 ± 4448 v. 2939 ± 784; small intestine: 1330 ± 573 v. 437 ± 171; muscle: 9861 ± 3640 v. 7907 ± 3229; spinal cord: 3961 ± 1819 v. 2756 ± 496). The variability of mtDNA copy number in clones was significantly higher in the lung, spleen, kidney, small intestine, and spinal cord (P = 0.001, 0.026, 0.005, 0.021, and 0.014, respectively; F-test), but not in other tissues. Methylation of the ANT4 gene is quite tissue dependent: hypomethylated in the liver, muscle and spinal cord; moderately methylated in the heart, lung, and kidney; and highly methylated in the spleen and small intestine. The methylation patters of ANT4 were not different between clones and non-clones. These results suggest that mtDNA copy number is more influenced by nongenetic factors than genetic background.
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Guo, Wenjun, Sunil Kumar, Frederik Görlitz, Edwin Garcia, Yuriy Alexandrov, Ian Munro, Douglas J. Kelly, et al. "Automated Fluorescence Lifetime Imaging High-Content Analysis of Förster Resonance Energy Transfer between Endogenously Labeled Kinetochore Proteins in Live Budding Yeast Cells." SLAS TECHNOLOGY: Translating Life Sciences Innovation 24, no. 3 (January 10, 2019): 308–20. http://dx.doi.org/10.1177/2472630318819240.
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We describe an open-source automated multiwell plate fluorescence lifetime imaging (FLIM) methodology to read out Förster resonance energy transfer (FRET) between fluorescent proteins (FPs) labeling endogenous kinetochore proteins (KPs) in live budding yeast cells. The low copy number of many KPs and their small spatial extent present significant challenges for the quantification of donor fluorescence lifetime in the presence of significant cellular autofluorescence and photobleaching. Automated FLIM data acquisition was controlled by µManager and incorporated wide-field time-gated imaging with optical sectioning to reduce background fluorescence. For data analysis, we used custom MATLAB-based software tools to perform kinetochore foci segmentation and local cellular background subtraction and fitted the fluorescence lifetime data using the open-source FLIMfit software. We validated the methodology using endogenous KPs labeled with mTurquoise2 FP and/or yellow FP and measured the donor fluorescence lifetimes for foci comprising 32 kinetochores with KP copy numbers as low as ~2 per kinetochore under an average labeling efficiency of 50%. We observed changes of median donor lifetime ≥250 ps for KPs known to form dimers. Thus, this FLIM high-content analysis platform enables the screening of relatively low-copy-number endogenous protein–protein interactions at spatially confined macromolecular complexes.
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Daher, May, Kai Cao, Rafet Basar, David Marin, Takuye Sekine, Gabriela Rondon, Weicheng Zhao, et al. "Donor NKG2C Copy Number: An Independent Predictor for CMV Reactivation after Double Cord Blood Transplantation." Blood 132, Supplement 1 (November 29, 2018): 2077. http://dx.doi.org/10.1182/blood-2018-99-114407.
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Abstract Cytomegalovirus (CMV) is a member of the herpesviridae family and remains latent in the host cells after primary infection. The virus reactivates in the immunosuppressed host and is a leading cause of morbidity following allogeneic hematopoietic stem cell transplant (allo-HSCT). Natural killer (NK) cells provide the first-line defence against viruses and a subset of NK cells expressing NKG2C have been shown to play a role in the immune surveillance of human CMV. Deletion of the NKG2C gene has been reported as a risk factor for viral infections including CMV and HIV, but current data on the influence of NKG2C gene-copy number variations in the donor graft on the risk of CMV reactivation after allo-HSCT is limited. Following cord blood transplantation (CBT), where the T-cell compartment is functionally naïve, the NKG2C genotype may have an even more pronounced impact on the risk of CMV reactivation. Therefore, we studied NKG2C copy number in the donor graft and the risk of CMV reactivation after double umbilical cord blood transplantation (DUCBT) in 100 CMV seropositive DUCBT recipients and their corresponding cord blood grafts (n=200). The gene encoding NKG2C is present at different copy numbers in the genomes of different individuals, with possible genotypes including 2 copies (wt/wt), 1 copy due to heterozygous deletion (wt/del) or 0 copies due to homozygous deletion (del/del). Among the donor CB units, approximately 2/3 had both copies of the gene (wt/wt), 1/3 had only one copy (wt/del) and only a minority of units had 0 copies with both alleles deleted (del/del). In the setting of DUCBT, the combined graft may contain 0 to 4 functional copies of NKG2C gene. In our cohort, patients whose combined grafts contained only 1 or 2 NKG2C gene copies had a significantly higher probability of CMV reactivation than patients whose combined grafts had 3 or 4 NKG2C copies. The 6-month cumulative incidence of CMV reactivation for the 4 groups was 100%, 92.9%, 60.5% and 55.9% respectively (p=0.005). No patient received a graft with zero gene copies. For the rest of the analysis we divided the patients into two groups, namely the 84 patients who received a combined graft with 3 or 4 NKG2C copies and the 16 patients who received two units with 1 or 2 NKG2C copies. The 6-month cumulative incidence of CMV reactivation for the two groups was 58.4% and 93.7% respectively (p=0.0003). In a multivariate analysis, receiving a combined graft with low NKG2C copy number (1 or 2 copies) (HR=2.72, CI=1.59-4.64; p<0.0001) and reduced intensity conditioning (RIC) (HR=0.59, CI=0.35-0.99, p=0.046) were the only independent predictors for CMV reactivation. Interestingly, the NKG2C copy number of the dominant cord was not predictive for CMV reactivation, suggesting that both cord blood units contribute to the antiviral response early post-DUCBT. Our study points to an important role for donor NKG2C in protection against CMV reactivation after DUCBT. If confirmed in larger numbers of CBT recipients, NKG2C genotyping of the CB graft may be a useful biomarker for predicting the risk of CMV infection after CBT, thus guiding the intensity of CMV prophylaxis for individual patients. Moreover these novel findings may provide a compelling rationale for considering NKG2C genotype as a criterion in the algorithm of CB selection for DUCBT. Disclosures Oran: ASTEX: Research Funding; AROG pharmaceuticals: Research Funding; Celgene: Consultancy, Research Funding. Champlin:Sanofi: Research Funding; Otsuka: Research Funding. Shpall:Affirmed GmbH: Research Funding.
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Jan, Max, Matthew J. Leventhal, Elizabeth A. Morgan, Jordan C. Wengrod, Anwesha Nag, Samantha D. Drinan, Bruce M. Wollison, et al. "Recurrent genetic HLA loss in AML relapsed after matched unrelated allogeneic hematopoietic cell transplantation." Blood Advances 3, no. 14 (July 19, 2019): 2199–204. http://dx.doi.org/10.1182/bloodadvances.2019000445.
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Abstract Immune evasion is a hallmark of cancer and a central mechanism underlying acquired resistance to immune therapy. In allogeneic hematopoietic cell transplantation (alloHCT), late relapses can arise after prolonged alloreactive T-cell control, but the molecular mechanisms of immune escape remain unclear. To identify mechanisms of immune evasion, we performed a genetic analysis of serial samples from 25 patients with myeloid malignancies who relapsed ≥1 year after alloHCT. Using targeted sequencing and microarray analysis to determine HLA allele-specific copy number, we identified copy-neutral loss of heterozygosity events and focal deletions spanning class 1 HLA genes in 2 of 12 recipients of matched unrelated-donor HCT and in 1 of 4 recipients of mismatched unrelated-donor HCT. Relapsed clones, although highly related to their antecedent pretransplantation malignancies, frequently acquired additional mutations in transcription factors and mitogenic signaling genes. Previously, the study of relapse after haploidentical HCT established the paradigm of immune evasion via loss of mismatched HLA. Here, in the context of matched unrelated-donor HCT, HLA loss provides genetic evidence that allogeneic immune recognition may be mediated by minor histocompatibility antigens and suggests opportunities for novel immunologic approaches for relapse prevention.
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Bétermier, Mireille, Sandra Duharcourt, Hervé Seitz, and Eric Meyer. "Timing of Developmentally Programmed Excision and Circularization of Paramecium Internal Eliminated Sequences." Molecular and Cellular Biology 20, no. 5 (March 1, 2000): 1553–61. http://dx.doi.org/10.1128/mcb.20.5.1553-1561.2000.
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ABSTRACT Paramecium internal eliminated sequences (IESs) are short AT-rich DNA elements that are precisely eliminated from the germ line genome during development of the somatic macronucleus. They are flanked by one 5′-TA-3′ dinucleotide on each side, a single copy of which remains at the donor site after excision. The timing of their excision was examined in synchronized conjugating cells by quantitative PCR. Significant amplification of the germ line genome was observed prior to IES excision, which starts 12 to 14 h after initiation of conjugation and extends over a 2- to 4-h period. Following excision, two IESs were shown to form extrachromosomal circles that can be readily detected on Southern blots of genomic DNA from cells undergoing macronuclear development. On these circular molecules, covalently joined IES ends are separated by one copy of the flanking 5′-TA-3′ repeat. The similar structures of the junctions formed on the excised and donor molecules point to a central role for this dinucleotide in IES excision.
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Faridi, Rehan Mujeeb, Taylor J. Kemp, Poonam Dharmani, Victor A. Lewis, Noureddine Berka, Jan Storek, and Faisal M. Khan. "Copies of Donor Killer Immunoglobulin-like Receptor Genes and Motifs Titrate Natural Killer (NK) Cells' Functional Response to Epstein - Barr Virus Infections and Influence the Risk of Developing Post-Transplant Lymphoproliferative Disease (PTLD) after Allogeneic Hematopoietic Cell Transplantation." Blood 126, no. 23 (December 3, 2015): 741. http://dx.doi.org/10.1182/blood.v126.23.741.741.
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Abstract BACKGROUND: Recipientsof allogeneic HCT remain vulnerable to a heightened risk of reactivation of otherwise latent viral infections owing to a compromised immune system early after transplantation. Uncontrolled reactivation of Epstein-Barr virus (EBV) leading to post-transplant lymphoproliferative disorder (PTLD) is one of such major complications after T-cell depleted HCT. Recovering within weeks after transplantation and being first in line of defense against viral infections, natural killer (NK) cells are deemed important in the immunopathogenesis of EBV complications. Their role however remains elusive. NK cell responses are regulated by a series of activating and inhibitory cell surface receptors, central to which are the Killer Immunoglobulin-like Receptors (KIR). Through these receptors NK cells discriminate healthy cells from 'altered' self-cells by scaling the perturbations in HLA expression after viral transformation of the target cell. Here, we set out to determine whether and how KIR gene and motifs' content of HCT donors and/or recipients influences the development of PTLD after allo-HCT. STUDY DESIGN: Hypothesizing that diverse NK cell receptor repertoires can titrate NK cell functional responses to EBV infections/reactivation and can potentially modify the risk of developing PTLD, we determined the KIR gene repertoires of 356 HLA-matched donor-recipient pairs of first allo-HCT and 50 healthy donors through Next Generation Sequencing of the KIR locus on the Illumina MiSeq platform. Based on the presence/absence and number of copies of individual genes, the KIR genotypes were determined and classified into four common centromeric (cA01, cB01, cB02 and cB03) and two telomeric (tA01 and tB01) motifs along with their variants. PBMNCs from KIR typed healthy volunteers were stimulated with EBV-transformed target cells to enumerate NK cell response to EBV (degranulation and/or IFNγ production) as a function of KIR gene content and motifs' distribution using a multicolor flow cytometry-based assay. Effect of KIR gene profile on development of PTLD was analyzed using binomial competing risks regression statistics. Distribution of NK cell functional response across various KIR characterized groups was analyzed using Mann-Whitney U statistics. RESULTS: Donor telomeric A motifs (tA01, KIR3DL1+ve KIR2DS4+ve; KIR3DS1/2DS1+/-ve), strongly protected against PTLD (p=0.0001, SHR=0.17; Figure 1). An increased protection against PTLD with increasing number of tA01 was noted with at least one copy required for a significant protective effect (Figure 1B). Copy number analysis of tA01 gene contents yielded similar associations. Further, the number of EBV induced functional NK cell subsets were significantly higher in individuals with than without KIR genotypes containing tA01 motifs (Figure 2 A-C) and was found to be increasing with an increasing number of tA01 copies (Figure 2 A'-C'). There was no influence of recipients' KIR repertoire on the risk of developing PTLD CONCLUSIONS: NK cell responsiveness, a function of KIR gene repertoire has a profound effect on the development of PTLD. Appropriately characterized KIR gene profile based identification of HCT recipients at high risk of developing PTLD will enable closer monitoring of EBV DNAemia and facilitate prompt therapy. Figure 1. Donor KIR telomeric A motif (tA01) protects against the risk of developing PTLD (A). Presence of at least one copy of donor KIR tA01 motif confers significant protection from PTLD (B) Figure 1. Donor KIR telomeric A motif (tA01) protects against the risk of developing PTLD (A). Presence of at least one copy of donor KIR tA01 motif confers significant protection from PTLD (B) Figure 2. KIR telomeric A motifs (tA01) titrate NK cells' functional response to Epstein-Barr virus infected cells (A-C), with and increasing %functional NK cells and subsets (measures as expressing CD107a, IFN-γ, or both) are observed with increasing tA01 motifs' copies (A'-C') Figure 2. KIR telomeric A motifs (tA01) titrate NK cells' functional response to Epstein-Barr virus infected cells (A-C), with and increasing %functional NK cells and subsets (measures as expressing CD107a, IFN-γ, or both) are observed with increasing tA01 motifs' copies (A'-C') Disclosures No relevant conflicts of interest to declare.
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Lee, TH, E. Donegan, S. Slichter, and MP Busch. "Transient increase in circulating donor leukocytes after allogeneic transfusions in immunocompetent recipients compatible with donor cell proliferation." Blood 85, no. 5 (March 1, 1995): 1207–14. http://dx.doi.org/10.1182/blood.v85.5.1207.bloodjournal8551207.
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Donor leukocytes in therapeutic blood components are implicated in transfusion-related complications ranging from alloimmunization to graft-versus-host disease (GVHD) to viral transmission and reactivation. To further characterize the kinetics of donor leukocyte clearance after allogeneic transfusion, we developed allele-specific polymerase chain reaction (PCR) assays directed at a single-copy Y chromosome gene and HLA class II alleles. These assays enable sensitive detection and quantitation of donor leukocytes at concentrations ranging from one cell to greater than 1,000 cells per 125 microL of recipient blood. When applied to serial samples from five consecutive orthopedic surgery patients who met study criteria, we observed 99.9% clearance of donor leukocytes over the initial 2 days posttransfusion, followed by a transient, 1-log increase in circulating donor leukocytes on days 3 to 5. This phenomenon was reproduced in a canine transfusion model, where the transient donor leukocyte expansion phase was prevented by gamma irradiation of donor blood, and was not observed after transfusions into alloimmunized dogs. We hypothesize that this transient increase in circulating allogeneic donor cells represents one arm of an in vivo mixed lymphocyte reaction, with activated donor T lymphocytes proliferating in an abortive GVHD reaction to HLA- incompatible recipient cells. Further investigation of this phenomenon should provide insight into the mechanisms involved in donor-recipient leukocyte interactions posttransfusion and the relationship of these interactions to leukocyte-induced complications.
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Flesch, Brigitte Katharina, Vanessa Scherer, Burkhard Just, Andreas Opitz, Oswin Ochmann, Anne Janson, Monika Steitz, and Thomas Zeiler. "Molecular Blood Group Screening in Donors from Arabian Countries and Iran Using High-Throughput MALDI-TOF Mass Spectrometry and PCR-SSP." Transfusion Medicine and Hemotherapy 47, no. 5 (2020): 396–408. http://dx.doi.org/10.1159/000505495.
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Background and Aims: Only little is known about blood groups other than ABO blood groups and Rhesus factors in Arabian countries and Iran. During the last years, increased migration to Central Europe has put a focus on the question how to guarantee blood supply for patients from these countries, particularly because hemoglobinopathies with the need of regular blood support are more frequent in patients from that region. Therefore, blood group allele frequencies should be determined in individuals from Arabian countries and Iran by molecular typing and compared to a German rare donor panel. Methods: 1,111 samples including 800 individuals from Syria, 147 from Iran, 123 from the Arabian Peninsula, and 41 from Northern African countries were included in a MALDI-TOF MS assay to detect polymorphisms coding for Kk, Fy(a/b), Fynull, Cw, Jk(a/b), Jo(a+/a–), Lu(a/b), Lu(8/14), Ss, Do(a/b), Co(a/b), In(a/b), Js(a/b), Kp(a/b), and variant alleles RHCE*c.697C>G and RHCE*c.733C>G. Yt(a/b), S–s–U–, Velnull, Conull, and RHCE*c.667G>T were tested by PCR-SSP. Results: Of the Arabian donors, 2% were homozygous for the FY*02.01N allele (Fynull), and 15.7% carried the heterozygous mutation. However, 0.8% of the German donors also carried 1 copy of the allele. 3.6% of all and 29.3% of Northern African donors were heterozygous for the RHCE*c.733C>G substitution, 0.4% of the Syrian probands were heterozygous for DO*01/DO*01.-05, a genotype that was lacking in German donors. Whereas the KEL*02.06 allele coding for the Js(a) phenotype was missing in Germans; 0.8% of the Syrian donors carried 1 copy of this allele. 1.8% of the Syrian but only 0.3% of the German donors were negative for YT*01. One donor from Northern Africa homozygously carried the GYPB*270+5g>tmutation, inducing the S–s–U+w phenotype, and in 2 German donors a GYPB*c.161G>A exchange, which induces the Mit+ phenotype, caused a GYPB*03 allele dropout in the MALDI assay. The overall failure rate of the Arabian panel was 0.4%. Conclusions: Some blood group alleles that are largely lacking in Europeans but had been described in African individuals are present in Arabian populations at a somewhat lower frequency. In single cases, it could be challenging to provide immunized Arabian patients with compatible blood.
Books on the topic "(donor) (copy 2)"
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Jean, Stafford. The collected stories of Jean Stafford. Austin: University of Texas Press, 1992.
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Jean, Stafford. The collected stories of Jean Stafford. New York: Farrar, Straus and Giroux, 2005.
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Lewis, Carroll. The Complete Alice in Wonderland. In 2 Vol. Macmillan Children's Books, 2007.
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Lewis, Carroll, and John Tenniel. Alices Abenteuer. 2 Bände. Alice im Wunderland / Alice hinter den Spiegeln. Insel, Frankfurt, 1998.
Find full textBook chapters on the topic "(donor) (copy 2)"
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Hopkins, P., and K. McNeil. "Lung transplantation." In Oxford Textbook of Medicine, 3476–85. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.1816_update_002.
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Lung transplantation offers the only therapeutic option for many patients with a variety of endstage pulmonary and cardiopulmonary diseases, but donors are scarce and the major challenge facing lung transplantation (as with all solid organ transplants) is the critical shortage of donor organs. Recipient selection—emphysema/chronic obstructive pulmonary disease (COPD), cystic fibrosis, idiopathic pulmonary fibrosis, and pulmonary vascular disease are the main disease groups referred for lung transplantation. Most patients are listed for transplantation when their survival is estimated to be less than 2 years without a transplant. Exclusion criteria include malignancy (excluding localized skin malignancies) within the last 2 years, inability to cooperate or comply with medical therapy/instruction, recent substance addiction, active or noncurable extrapulmonary infection, significant chest wall/spinal deformity, and significant extrathoracic organ dysfunction....