Academic literature on the topic 'B-CLL'
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Journal articles on the topic "B-CLL"
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Parker, Anton, Shilu Amin, Tricia Zwiefelhofer, et al. "Epigenetic Regulation of ZAP70 in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (2008): 2246. http://dx.doi.org/10.1182/blood.v112.11.2246.2246.
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Abstract ZAP70 expression has been shown to be involved in enhanced signalling and more aggressive disease in a subset of CLL. Mechanisms regulating ZAP70 expression are unknown. We have shown previously that despite the absence of a 5’ CpG island, the methylation status of a small region of CpG dinucleotides (CpGs) correlates with the transcriptional state of the gene in both normal lymphocytes and B cell leukemias. Quantitative methylation analysis of 605 CpGs across the 28kb genomic region spanning ZAP70 was performed by MassARRAY on a panel of 17 CLL tumor cell samples, 4 lymphoid cell lines and B cell, T cell and myeloid cell samples pooled from 3 normal individuals. All samples showed hypermethylation of the gene body and of the gene’s two 3’ CpG islands. However, there was variability between samples in the methylation of 12 consecutive CpGs within a 1kb predicted promoter region (PPR), spanning the transcription start site (TSS) and in the methylation of 24 consecutive CpGs in an adjacent 1kb differentially methylated region (DMR), downstream of the TSS. The methylation of the PPR and DMR, together with the expression status of the samples, suggested four different states for the gene (Table 1). Table 1 - ZAP70 gene states defined by ZAP70 expression status and methylation of the PPR and DMR. MEAN CpG METHYLATION (%) SAMPLE ZAP70 EXPRESSION STATUS PPR DMR GENE STATE NAMALWA − 65 82 I B CELLS − 48 82 I MYELOID − 53 80 I CLL6 − 4 86 II CLL7 − 5 75 II CLL8 − 12 78 II CLL10 − 12 62 II CLL11 − 4 62 II CLL12 − 21 77 II HBL2 − 18 60 II CLL13 + 4 40 III CLL14 + 5 46 III CLL15 + 7 45 III CLL16 + 9 43 III CLL17 + 5 56 III NALM6 + 8 52 III CLL1 + 3 4 IV CLL2 + 3 4 IV CLL9 + 4 6 IV CLL4 + 3 8 IV CLL5 + 4 16 IV CLL3 + 4 17 IV JURKAT + 3 4 IV T CELLS + 9 13 IV Bisulphite cloning and sequencing of a PCR amplicon spanning an exon1 C/A SNP (rs2276645) and the PPR/DMR junction was performed together with cDNA pyrosequencing of rs2276645 on the five CLL tumor samples identified with gene state III. All samples showed allele specific methylation (ASM) of the A allele within the DMR and almost complete restriction of ZAP70 expression to the hypomethylated C allele. Bisulphite pyrosequencing of two DMR CpGs in purified leukocyte populations from these cases showed that ASM appears restricted to CLL cells, with hypermethylation and hypomethylation of the myeloid and T cells respectively (Table2). This suggests that while methylation of the DMR is sufficient for allele restriction, ASM does not result from imprinting and may be restricted to CLL tumor cells. Table 2 – Mean methylation of 2 DMR CpGs in leukocyte populations from CLL patients with known ASM of the DMR in their tumor cells. MYELOID CELLS CLL CELLS T CELLS PATIENT CD15 (%) METHYLATION(%) CD19 (%) METHYLATION (%) CD2 (%) METHYLATION (%) CLL13 83 90 98 59 71 21 CLL14 98 99 98 50 88 10 CLL15 88 84 93 45 85 24 CLL16 99 96 99 52 82 18 CLL17 92 89 98 49 90 22 Native chromatin immunoprecipitation (N-ChIP) using anti-AcH3, H3K14Ac and H3K14Me2 antibodies was performed on the 4 cell lines and tumor cells from CLLs 1, 2, 6, 7, 13 and 14 from the MassARRAY series. PCR for amplicons across the PPR and DMR showed the presence of all 3 histone modifications in ZAP70 expressing JURKAT and NALM6 cells but these modifications were absent in the ZAP70 negative NAMALWA and HBL2 cells. In contrast, all 6 CLL samples showed enrichment for all 3 modifications, regardless of gene state, suggesting an open, active/permissive chromatin structure, despite clear differences in methylation of the DMR. Further bisulphite pyrosequencing and N-ChIP of NAMALWA and HBL2 cells cultured for 6 days in the presence of 0.5μM Decitibine showed concomitant DMR demethyaltion, increased AcH3 within the DMR and up regulation of ZAP70 expression, all of which were reversed when the drug stimulus was removed. Taken together this data suggests that ZAP70 is regulated by epigenetic mechanisms, with the methylation status of a small DMR playing a key role, sufficient to differentiate the transcriptional activity of two alleles within a single cell. It is apparent that the gene is primed for expression in all CLL cells and that methylation of the DMR is part of the key switching process between active transcription and silencing. The differences in DMR methylation between an individual’s expressing T cells and CLL cells, suggests that differences may exist in the mechanism of regulation between T and B cells and raises the possibility that such differences could be exploited as targets for therapy.
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Silber, R., CM Farber, E. Papadopoulos, et al. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.
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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., CM Farber, E. Papadopoulos, et al. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.
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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Goodman, Alice. "B-CLL." Oncology Times &NA;, Supplement (2006): 21. http://dx.doi.org/10.1097/01.cot.0000316106.04463.a9.
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Silber, R., B. Degar, D. Costin, et al. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.3440.
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Abstract Chemosensitivity of B lymphocytes, obtained from 65 patients with B- cell chronic lymphocytic leukemia (B-CLL), Rai stages 0 through IV, was determined using the MTT assay. The results were expressed by the drug concentration required for 50% inhibition of cell viability (IC50). The cytotoxicity of chlorambucil (CLB) was compared with that of fludarabine and the DNA topoisomerase I inhibitors, camptothecin, 9- aminocamptothecin, 10,11-methylenedioxy-20(S)-camptothecin (10,11-MDC) and 9-amino-10,11-methylenedioxy-20(S)-campthothecin (9-A-10,11-MDC), and topotecan. Considerable heterogeneity in sensitivity to CLB was observed, with a median IC50 of 40.5 mumol/L in untreated patients. B- CLL cells from patients treated with CLB had a significantly higher median IC50 of 86.0 mumol/L (P < .01). Untreated as well as CLB-treated patients were divided into two subsets. For the purpose of this study, B-CLL lymphocytes with an IC50 CLB of less than 61.0 mumol/L were designated as “sensitive” and those with an IC50 CLB of > or = 61.0 mumol/L were designated as “0resistant.” After baseline assays, 15 untreated patients received CLB; after treatment, the IC50 increased in B-CLL lymphocytes from 13 of 15 patients. The response to CLB treatment, determined by its effect on the absolute lymphocyte count and by the Eastern Cooperative Oncology Group clinical criteria, was significantly better in patients whose lymphocytes had an IC50 CLB of less than 61.0 mumol/L before therapy (P < .01). B-CLL lymphocytes also had a variable degree of sensitivity in vitro to each of the other drugs. There was significant cross-resistance between CLB and fludarabine (P < 0.01). Whereas only 29% of CLB-resistant B-lymphocyte specimens obtained from individual patients were sensitive to fludarabine in vitro, 52% and 67% of CLB-resistant lymphocyte samples were sensitive to 10,11-MDC and 9-A-10,11-MDC, respectively. We have previously reported that p53 gene mutations were associated with aggressive B-CLL and a poor prognosis. B lymphocytes from seven patients with these mutations were resistant to CLB, and five of six were resistant to fludarabine. Lymphocytes from four of seven were resistant to 10,11-MDC, and three of four were resistant to 9-A-10,11- MDC. This study implies that the MTT assay may be useful in identifying subsets of CLL patients resistant to conventional chemotherapy. However, definitive conclusions can not be drawn in view of the small number of patients studied prospectively. In addition, these results suggest the potential of camptothecin-based therapy for patients unresponsive to standard treatment.
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Silber, R., B. Degar, D. Costin, et al. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.bloodjournal84103440.
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Chemosensitivity of B lymphocytes, obtained from 65 patients with B- cell chronic lymphocytic leukemia (B-CLL), Rai stages 0 through IV, was determined using the MTT assay. The results were expressed by the drug concentration required for 50% inhibition of cell viability (IC50). The cytotoxicity of chlorambucil (CLB) was compared with that of fludarabine and the DNA topoisomerase I inhibitors, camptothecin, 9- aminocamptothecin, 10,11-methylenedioxy-20(S)-camptothecin (10,11-MDC) and 9-amino-10,11-methylenedioxy-20(S)-campthothecin (9-A-10,11-MDC), and topotecan. Considerable heterogeneity in sensitivity to CLB was observed, with a median IC50 of 40.5 mumol/L in untreated patients. B- CLL cells from patients treated with CLB had a significantly higher median IC50 of 86.0 mumol/L (P < .01). Untreated as well as CLB-treated patients were divided into two subsets. For the purpose of this study, B-CLL lymphocytes with an IC50 CLB of less than 61.0 mumol/L were designated as “sensitive” and those with an IC50 CLB of > or = 61.0 mumol/L were designated as “0resistant.” After baseline assays, 15 untreated patients received CLB; after treatment, the IC50 increased in B-CLL lymphocytes from 13 of 15 patients. The response to CLB treatment, determined by its effect on the absolute lymphocyte count and by the Eastern Cooperative Oncology Group clinical criteria, was significantly better in patients whose lymphocytes had an IC50 CLB of less than 61.0 mumol/L before therapy (P < .01). B-CLL lymphocytes also had a variable degree of sensitivity in vitro to each of the other drugs. There was significant cross-resistance between CLB and fludarabine (P < 0.01). Whereas only 29% of CLB-resistant B-lymphocyte specimens obtained from individual patients were sensitive to fludarabine in vitro, 52% and 67% of CLB-resistant lymphocyte samples were sensitive to 10,11-MDC and 9-A-10,11-MDC, respectively. We have previously reported that p53 gene mutations were associated with aggressive B-CLL and a poor prognosis. B lymphocytes from seven patients with these mutations were resistant to CLB, and five of six were resistant to fludarabine. Lymphocytes from four of seven were resistant to 10,11-MDC, and three of four were resistant to 9-A-10,11- MDC. This study implies that the MTT assay may be useful in identifying subsets of CLL patients resistant to conventional chemotherapy. However, definitive conclusions can not be drawn in view of the small number of patients studied prospectively. In addition, these results suggest the potential of camptothecin-based therapy for patients unresponsive to standard treatment.
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Matvieieva, A. S., L. M. Kovalevska, and E. V. Kashuba. "The SMAD4 transcription factor shows cytoplasmic retention in B-cells of patients with chronic lymphocytic leukemia (CLL)." Faktori eksperimental'noi evolucii organizmiv 22 (September 9, 2018): 144–48. http://dx.doi.org/10.7124/feeo.v22.939.
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Aim. To illuminate the reason of inactivity of the TGFB-SMAD2/3 pathways in CLL cells. Methods. CLL cells were isolated from peripheral blood of CLL patients, using gradient centrifugation at the ficoll. Expression and cellular localization of SMAD2, 3 and 4 proteins were analyzed by fluorescence microscopy, using specific antibodies. Results. The SMAD2 protein was basically not expressed in CLL cells, in contrast to B cells, isolated from the peripheral blood of a healthy donor. Moreover, the SMAD3 and SMAD4 proteins were localized exclusively in the cytoplasm (a proportion of SMAD3 was detected in the membrane) of CLL cells. Conclusions. The TGFB-SMAD2/3 signaling pathway is not active in CLL cells. We have found that SMAD2 is not expressed. Also, the nuclear heterodimers that consisted of SMAD3 and SMAD4 proteins, were not detected.
 Keywords: chronic lymphocytic leukemia (CLA), acute myeloid leukemia (AML), peripheral blood B-cells, SMAD, the TGFB-SMAD2/3 signaling pathway.
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Santiago-Schwarz, F., C. Panagiotopoulos, A. Sawitsky, and KR Rai. "Distinct characteristics of lymphokine-activated killer (LAK) cells derived from patients with B-cell chronic lymphocytic leukemia (B-CLL). A factor in B-CLL serum promotes natural killer cell-like LAK cell growth." Blood 76, no. 7 (1990): 1355–60. http://dx.doi.org/10.1182/blood.v76.7.1355.1355.
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Abstract We show that lymphokine-activated killer (LAK) cell precursors derived from patients with B-cell chronic lymphocytic leukemia (B-CLL) and cultured in the presence of recombinant interleukin-2 and normal human serum (NHS), develop into primarily NK cell-like (CD 57+) LAK cells, whereas identically prepared LAK cell precursors from normal subjects develop into mainly T cell-like (CD 3+, CD 8+) LAK cells. B-CLL LAK cells exhibited greater proliferative capacity than did normal LAK cells. When normal LAK cells were grown in B-CLL serum instead of NHS, their proliferation increased; NK cell levels also increased to those found in B-CLL LAK cells, suggesting that B-CLL serum contains a factor that promotes NK cell-like growth, LAK cells derived from normal or B- CLL patients demonstrated similar lytic activity toward K562 and Raji cells. Growth in B-CLL serum did not reduce their lytic potential. Thus, the altered phenotype and growth exhibited by B-CLL LAK cells and normal LAK cells grown in B-CLL serum does not lead to abnormalities in their cytolytic functions. We propose instead that the predominance of NK-like cells in B-CLL LAK cell populations and the presence of an NK cell-like growth factor in B-CLL serum reflect abnormalities related to NK cell-mediated B-cell regulation; ie, either inhibition of normal B- cell growth and/or growth stimulation of the leukemic clone in B-CLL.
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Santiago-Schwarz, F., C. Panagiotopoulos, A. Sawitsky, and KR Rai. "Distinct characteristics of lymphokine-activated killer (LAK) cells derived from patients with B-cell chronic lymphocytic leukemia (B-CLL). A factor in B-CLL serum promotes natural killer cell-like LAK cell growth." Blood 76, no. 7 (1990): 1355–60. http://dx.doi.org/10.1182/blood.v76.7.1355.bloodjournal7671355.
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We show that lymphokine-activated killer (LAK) cell precursors derived from patients with B-cell chronic lymphocytic leukemia (B-CLL) and cultured in the presence of recombinant interleukin-2 and normal human serum (NHS), develop into primarily NK cell-like (CD 57+) LAK cells, whereas identically prepared LAK cell precursors from normal subjects develop into mainly T cell-like (CD 3+, CD 8+) LAK cells. B-CLL LAK cells exhibited greater proliferative capacity than did normal LAK cells. When normal LAK cells were grown in B-CLL serum instead of NHS, their proliferation increased; NK cell levels also increased to those found in B-CLL LAK cells, suggesting that B-CLL serum contains a factor that promotes NK cell-like growth, LAK cells derived from normal or B- CLL patients demonstrated similar lytic activity toward K562 and Raji cells. Growth in B-CLL serum did not reduce their lytic potential. Thus, the altered phenotype and growth exhibited by B-CLL LAK cells and normal LAK cells grown in B-CLL serum does not lead to abnormalities in their cytolytic functions. We propose instead that the predominance of NK-like cells in B-CLL LAK cell populations and the presence of an NK cell-like growth factor in B-CLL serum reflect abnormalities related to NK cell-mediated B-cell regulation; ie, either inhibition of normal B- cell growth and/or growth stimulation of the leukemic clone in B-CLL.
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Tummala, Hemanth, Alexey Goltsov, Hilal S. Khalil, et al. "Advocating the need of a systems biology approach for personalised prognosis and treatment of B-CLL patients." BioDiscovery 6 (December 30, 2012): e8939. https://doi.org/10.7750/BioDiscovery.2012.6.4.
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The clinical course of B-CLL is heterogeneous. This heterogeneity leads to a clinical dilemma: can we identify those patients who will benefit from early treatment and predict the survival? In recent years, mathematical modelling has contributed significantly in understanding the complexity of diseases. In order to build a mathematical model for determining prognosis of B-CLL one has to identify, characterise and quantify key molecules involved in the disease. Here we discuss the need and role of mathematical modelling in predicting B-CLL disease pathogenesis and suggest a new systems biology approach for a personalised therapy of B-CLL patients.
Dissertations / Theses on the topic "B-CLL"
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Schlaak, Max Simon. "Differentielles Genexpressionsmuster in chronischen lymphatischen Leukämiezellen vom B-Zell-Typ (B-CLL-Zellen)." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=966320069.
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Schlaak, Max Simon. "Differentielles Genexpressionsmuster in chronischen lymphatischen Leukämiezellen vom B-Zell-Typ (B-CLL-Zellen)." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14817.
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Die B-CLL ist eine niedrigmaligne Erkrankung, die im höheren Lebensalter auftritt und für die es weiterhin keine dauerhaft kurative Therapie gibt. Die Erforschung der genetischen Grundlagen dieser Krankheit könnte Erkenntnisse über die Funktionsmechanismen und neue Diagnose- und Therapieansätze erbringen. Ziel dieser Arbeit war es, eine Genbank von CLL-Patienten bzw. gesunden Spendern zu erstellen, um Gene, die für die Entstehung der Erkrankung mitverantwortlich sein könnten, zu identifizieren. Die subtraktive suppressive Hybridisierung (SSH) wurde als Methode eingesetzt, um cDNA-Mischungen zu generieren, in denen differentielle Gene angereichert wurden. In dieser Arbeit wurden drei differentielle Gene identifiziert. Eines dieser Gene kodiert den Oberflächenmarker CD5, der bei CLL-Erkrankten stärker exprimiert wurde. Da CD5 ein für die B-CLL relativ spezifischer Marker ist, bestätigte dieses Ergebnis die Qualität der Genbank. Mit Hilfe der SSH wurde ein Verlust der Expression der cDNA für den Oberflächenmarker CD20 bei CLL-Erkrankten nachgewiesen. CD20 ist möglicherweise ein Kalziumkanal und wird als Ziel des anti-CD20-Antikörpers Rituximab verwendet. Der Verlust von CD20 im Verlauf der Erkrankung konnte in dieser Arbeit angedeutet werden. Weiterhin wurde eine verringerte Expression von cDNA für IkappaBa (Mad-3) bei CLL-Patienten entdeckt. Der Transkriptionsfaktor IkBa spielt im zellulären Ablauf der Apoptose eine wichtige Rolle. Phosphoryliertes IkBa inhibiert die Wirkung von NF-kB. Eine Reduktion von IkBa-cDNA könnte ebenfalls die Funktion von NF-kB beeinflussen. Dieses Ergebnis könnte auch für zukünftige immuntherapeutische Ansätze von Bedeutung sein. Weiterhin sind die nachgewiesenen Gene interessant für die Technik des "DNA-Microarrays". Diese schnelle Methode ermöglicht kostengünstige Diagnosen und könnte daher eine zukunftsweisende Alternative zu herkömmlichen Ansätzen bieten. In der vorliegenden Arbeit konnten differentielle Transkripte auf mRNA-Ebene bei B-CLL-Erkrankten und gesunden Kontrollen festgestellt und untersucht werden. Die Ergebnisse geben neue Einsichten über Onkogene und Tumorsurpressorgene in der B-CLL und eröffnen zukünftige immuntherapeutische Ansätze.<br>The B-CLL is a malignancy that appears in the higher age and for which it gives further no durably curative therapy. The investigation of the genetic bases of this illness could furnish understandings of the function mechanisms and new diagnosis and therapy extensions. It was the goal of this work of generating a gene bank of CLL-patients and healthy donors, in order to identify genes, that could be responsible for the origin of the disease. The subtractive suppressive hybridisation (SSH) was inserted as a method in order to generate cDNA-mixtures, in which differential genes were enriched. In this work, three differential genes were identified. One of these genes codes for CD5 that in CLL-patients was stronger expressed. Because CD5 is a marker relatively specific for the B-CLL, this result confirmed the quality of the gene bank. By means of the SSH, a loss of the Expression of the cDNA was proved for CD20 in CLL-patients. Possibly CD20 is a calcium canal and is used as a goal of the anti-CD20-antibody Rituximab. The loss of CD20 in the progress of the disease could be indicated in this work. Further a diminished expression was discovered by cDNA for IkBa (Mad-3) in CLL-patients. The transcription factor IkBa plays an important role in the cellular system of apoptosis. Phosphorylated IkBa is inhibiting the effect of NF-kB. A reduction of IkBa-cDNA could influence also the function of NF-kB. This result could be interesting for future immune therapeutic extension. Further the proved genes are interesting for the technology of the "DNA-Microarrays". This fast method enables favorable diagnoses and could offer therefore a leading-edge alternative to conventional extensions. In the existing work, differential transcripts could be assessed on mRNA-levels in B-CLL-patients and healthy donors. The results give new insights over oncogenes and tumor surpressing genes in the B-CLL and open future immune therapeutic extensions.
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Kurzeder, Christian. "Gentransfer in primäre B-CLL-Zellen mittels EBV abgeleiteter Genvektoren." [S.l.] : [s.n.], 2004. http://edoc.ub.uni-muenchen.de/archive/00004955.
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Kurzeder, Christian. "Gentransfer in primäre B-CLL-Zellen mittels EBV abgeleiteter Genvektoren." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-49552.
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Bund, Dagmar. "hTERT, CD23 und CD229 als Tumorantigene bei der B-CLL." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145282.
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Almond, Jason Baron. "Mechanisms of proteasome inhibitor-induced apoptosis of B-cell chronic lymphocytic leukaemia (B-CLL) cells." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/30761.
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Proteasome inhibitors, including lactacystin, LLnL (N-acetyl-N-leucinyl-L-leucinyl-L- norleucinal) and MG132 (carbobenzoxyl-leucinyl-leucinyl-leucinal), potently induce apoptosis in leukaemic B-cells from patients with B-cell chronic lymphocytic leukaemia (B-CLL). This pro-apoptotic effect occurs in cells from patients at all stages of the disease, including those resistant to conventional chemotherapy, suggesting that proteasome inhibitors may be useful for treatment of B-CLL. Following initial inhibition of proteasomal activity and an increase in ubiquitinated proteins, these agents induce mitochondrial cytochrome c release and caspase-dependent apoptosis, involving cleavage/activation of caspases -2, -3, -7, -8 and - 9. Pre-treatment with the cell permeable caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe)fluoromethyl ketone (Z-VAD.fmk), does not prevent the release of cytochrome c or partial processing of caspase-9 but prevents activation of effector caspases and induction of apoptosis. These results suggest that the release of cytochrome c is caspase independent and that caspase-9 is the initiator caspase in proteasome inhibitor-induced apoptosis of B-CLL cells. Activation of B-CLL lysates with dATP results in the formation of an -700 kDa caspase-activating apoptosome complex containing Apaf-1. A similar complex is formed in B-CLL cells induced to undergo apoptosis by proteasome inhibitors. Mechanisms of proteasome inhibitor-induced apoptosis vary between cell types, but often involve accumulation of short-lived proteins such as p53, p27 and pro-apoptotic Bcl-2 family members, activation of the stress kinase JNK, or inhibition of NF-kB transcriptional activity. Proteasome inhibitor-induced apoptosis in B-CLL cells is not triggered by alterations in the Bcl-2:Bax ratio, increase in pro-apoptotic t-Bid, or alterations in p27, XIAP, cIAPl or cIAP2. There is also no accumulation of IkB proteins that would inhibit NFkB survival signalling. Although proteasome inhibitors cause an accumulation of p53 and p21, this is not sufficient to induce apoptosis, as etoposide causes more pronounced increases in these molecules but is a less potent inducer of apoptosis. Activation of the stress kinases c-Jun N- terminal kinase (JNK) and p38 also does not appear to be involved. Therefore proteasome inhibitors induce mitochondrial perturbation in B-CLL cells by an apparently novel mechanism.
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Walton, Alexander James. "CD4+PF+ T Cells in B-CLL Patients & Normal Controls." Thesis, University of Westminster, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502405.
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Our group has previously shown that CD4+Perforin (PFt T cells with cytotoxic potential are expanded in patients with B-CLL, accounting for up to 50% of CD4+ T cells in this disease. This study confinns the finding of increased percentages of CD4+PF+ T cells in a new cohort of B-CLL patients. However, the significance of this subset in B-CLL remains unclear. Evidence has accumulated for the potential role of CD4+ cytotoxic T cells in controlling cytomegalovirus (CMV). Therefore, a potential relationship between chronic CMV infection and CD4+PF+ T cell expansion in B-CLL was investigated. CMV seropositivity was found to be strongly associated with CD4+PF+ T cell expansion in both B-CLL patients and controls. This suggested that CD4+PF+ T cells from CMV seropositive (SP) patients and controls might contain clonally expanded populations of CMV-specific cells. To test this hypothesis, the CMV reactivity of CD4+PF+ and CD4+PF- T cells from B-CLL patients and controls was detennined using an intracellular cytokine staining flow cytometric assay. CD4+PF+ cells from untreated patients were enriched for CMV-reactive cells, as measured by . IFN-y production, compared to the CD4+PF- subset. In addition, the data indicated that CD4+ T cell immunity to CMV is dysregulated in B-CLL patients. CD4+PF+T cells from B-CLL patients are characterised by a highly differentiated CD2S-CD57+ phenotype. To further characterise the differentiation phenotype of these cells, the distribution of CD45RA and CCR7 was detennined on CD4+PF+ T cells from B-CLL patients and controls. CD4+PF+ T cells from B-CLL patients were both characterised by a highly differentiated T-effector memory TEM (CCRT) phenotype, but differed in the proportion of CD45RA expressing cells, which might reflect chronic T cell activation in the fonner group. ~inally, flowFISH analysis revealed that CD4+PF+ T cells had shorter telomeres compared CD4+PF- T cells in B-CLL patients, indicative of a more extensive replicative history. The results indicate that low, but persistent, antigenic exposure in CMVinfected individuals leads to the emergence of a CD4+PF+ T cell subset, characterised by a highly differentiated cell surface phenotype and shortened telomeres.
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Munoz-Ritchie, Varinia Graciela. "P-glycoprotein-associated anthracycline resistance in B-CLL : potential for cytokine modulation." Thesis, University of Plymouth, 2001. http://hdl.handle.net/10026.1/2809.
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The phenomenon of multidrug resistance (MDR) in cancer cells is generally associated with P-glycoprotein (P-gp) expression and presents an obstacle to successful chemotherapy. Attempts to overcome P-gp-associated MDR using P-gp modulators, such as verapamil, have been hindered by their intrinsic in vivo toxicity. In 1991, however, Scala et al. demonstrated the alteration of P-gp function by interferon-alpha (IFN-α) in vitro at non-toxic in vivo concentrations, suggesting a basis for the use of IFN-α clinically in patients exhibiting P-gp-associated MDR. Drug resistance in B-CLL has been linked to the phenomenon of MDR, however, publications regarding this have been conflicting. The contrasting results prompted further investigation of the role of P-gp-associated anthracycline resistance and, using isolated β-lymphocytes from B-CLL patients, this investigation examined P-gp expression, function and IFN-α modulation in vitro. Optimum conditions for in vitro analysis of P-gp-associated anthracycline resistance were determined by examining the stability of the anthracycline, daunorubicin, in varying cell culture conditions. The resulting system balanced conditions affecting drug stability with those affecting cell survival. While other investigations have neglected the issue of drug stability, this study demonstrates that the instability of daunorubicin may be a critical variable determining the outcome of drug sensitivity studies. In RPMI + 2mM L-glutamine and 10% (v/v) FBS, loss of drug concentration is due to both adsorption and degradation and these experiments show that the presumed availability of drug may be over-estimated in in vitro studies. Furthermore, the degradation products might interfere with P-gp function and modulation. MDRl gene mRNA was detected in the B-cells of forty-three out of fifty B-CLL patients analysed, whereas P-gp expression, as measured by flow cytometry, resulted in only sixteen patients out of fifty-five being classed as positive (> 10% increase in staining as compared to the control). P-gp functionality and modulation studies on the B-cells of eleven patients confirmed the existence of an efflux mechanism with identical characteristics to P-gp using verapamil, the dye rhodamine 123 (rho123) and daunorubicin. Four patients were classed as functional low expressers (functional P-gp with low P-gp expression (7-10% increase in staining)), six were classed as functional high expressors (functional P-gp with high P-gp expression (20-57% increase in staining)) and one as a non-functional high expressor (non-functional P-gp with high P-gp expression (13.4% increase in staining)). Verapamil modulated rho123 efflux in all ten patients classed as P-gp functional expressors, and daunorubicin efflux in eight of these patients. However, IFN-α modulated rho123 and daunorubicin efflux in only two and one patients, respectively, even at concentrations higher than 500I.U./ml. In contrast to Scala et al. (1991), this finding suggests that at a well tolerated concentration IFN-α may not be suitable for use as a P-gp modulating agent in vivo in B-CLL, although conclusive evidence would require a larger study.
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Hellqvist, Eva. "Antigen interaction with B cells in two proliferative disorders : CLL and MGUS." Doctoral thesis, Linköping : Department of Clinical and Experimental Medicine, Linköping University, 2010. http://www2.bibl.liu.se/liupubl/disp/disp2010/med1158s.pdf.
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Gorgone, Ausilia Giuseppa. "Correlazione tra dati biologici e prognosi in pazieti affetti da B-CLL." Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1138.
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Gli studi di questi anni hanno dimostrato che i fattori biologici giocano un ruolo fondamentale per la stratificazione del rischio come elementi predittivi del treatment-free survival e dell' overall survival nei pazienti affetti da CLL in stadio iniziale.La maggioranza di questi markers prognostici ,anche se ormai in uso quotidiano nella pratica clinica, non è ancora incluso nelle linee guida internazionali che si basano ancora su criteri esclusivamente clinici e individuano la valutazione biologica da usare in combinazione ai parametri clinici.Il loro impiego può certamente contribuire al miglioramento del clinical management dei pazienti affetti da CLL .
Books on the topic "B-CLL"
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Dawson, Alma. Development of a core library collection for library automation: Report to the Council on Library Resources on Project CLR #4026-B. Produced at the Research Center Annex, School of Library and Information Science, Louisiana State University, 1989.
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Flohr, T. Regulation von Zytoinproduktion und Zellproliferation durch Zytokine bei B-CLL-Zellen in vitro. 2000.
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Brass, Ute. Der Einfluss von Interferon-alpha auf durch CD40-Antikörper stimulierte B-CLL-Zellen. 1996.
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Leukaemia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0004.
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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Hassan Al-Sader. Leukaemia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0004_update_001.
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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Magin, Thomas O. H. Durchflusszytometrische Immunphänotypisierung maligner B-CLL Lymphozyten: Korrelation zu Klinik und prognostischen Parametern der chronisch lymphatischen Leukämie. 1995.
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Woelke, Corinna. Ex-vivo Inkubation von immunomagnetisch aufgereinigten autologen Stammzelltransplantaten bie Patienten mit B-CLL zur Eliminierung residueller kontaminierender Tumorzellen. 2003.
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Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.
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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodysplastic syndromes (MDS), follicular lymphoma, diffuse large B-cell lymphoma, Burkitt’s lymphoma (BL), extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), mantle cell lymphoma, classical Hodgkin’s lymphoma (cHL), lymphoplasmacytic lymphoma (LPL), plasma cell myeloma, primary amyloidosis, and mature T-cell non-Hodgkin’s lymphomas.
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Steensma, David P. Malignant Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0296.
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The hematologic neoplasms include lymphoproliferative disorders (eg, chronic lymphocytic leukemia [CLL]/small lymphocytic lymphoma [SLL], large granular lymphocyte leukemia, hairy cell leukemia [HCL], Hodgkin lymphoma, non-Hodgkin lymphoma), plasma cell disorders (multiple myeloma, light chain amyloidosis, Waldenström macroglobulinemia, POEMS syndrome, heavy chain disease, plasmacytoma), chronic myeloid neoplasms (chronic myeloid leukemia, the BCR/ABL-negative myeloproliferative neoplasms, myelodysplastic syndromes), and acute leukemia (acute myeloid leukemia, acute lymphocytic leukemia). In addition, clonal but not overtly malignant conditions are common in the general population, including monoclonal gammopathy of undetermined significance (MGUS) and monoclonal B lymphocytosis (MBL).
Book chapters on the topic "B-CLL"
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Stilgenbauer, Stephan, Hartmut Döhner, and Peter Lichter. "Chronisch lymphatische Leukämie vom B-Zell-Typ (B-CLL)." In Molekularmedizinische Grundlagen von hämatologischen Neoplasien. Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59343-7_13.
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Agathangelidis, Andreas, Stavroula Ntoufa, and Kostas Stamatopoulos. "B Cell Receptor and Antigens in CLL." In Advances in Experimental Medicine and Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8051-8_1.
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Faguet, Guy B. "Clonal Evolution and Second Malignancies in B-CLL." In Chronic Lymphocytic Leukemia. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_21.
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Hamblin, Terry. "The Heterogeneous Origin of the B-CLL Cell." In Chronic Lymphocytic Leukemia. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_4.
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Genetet, Noelle, Dominique Bourel, Bernard Grosbois, et al. "Heterogeneity of B-CLL Cells Defined by Monoclonal Antibodies." In Leukocyte Typing II. Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4848-4_32.
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Schetelig, Johannes, and Peter Dreger. "Chronic Lymphocytic Leukemia." In The EBMT Handbook. Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_85.
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AbstractCLL is a rare indication for HCT/Cellular Therapy since it usually follows an indolent course. Allogeneic HCT is considered as standard of care in eligible high-risk patients who have failed at least two classes of modern pathway inhibitor-based therapy, and in select patients with CLL transformed in to an aggressive B-cell lymphoma (Richter transformation). Except for Richter transformation, there is no role for autologous HCT in CLL. In the absence of a labeled indication, CAR T-cells should not be used outside of clinical trials.
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Lanza, F., and G. L. Castoldi. "Flow Cytochemical Analysis of Lymphoid Cells in B-Chronic Lymphocytic Leukemia (B-CLL)." In Leukemias. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77083-8_56.
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Phipps, R. P., S. J. Pollock, K. Kaur, et al. "Expression of Cyclooxygenase-2 and Prostaglandins by B-1 Cells and B-CLL Cells." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_30.
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Okkenhaug, Klaus, and Jan A. Burger. "PI3K Signaling in Normal B Cells and Chronic Lymphocytic Leukemia (CLL)." In Current Topics in Microbiology and Immunology. Springer International Publishing, 2015. http://dx.doi.org/10.1007/82_2015_484.
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Gorczyca, Wojciech. "Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL) and B-Cell Prolymphocytic Leukemia (B-PLL)." In Atlas of Differential Diagnosis in Neoplastic Hematopathology, 4th ed. CRC Press, 2021. http://dx.doi.org/10.1201/9781003120445-09.
Full textConference papers on the topic "B-CLL"
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Chambers, Brian, Russ Kane, and Mark Yunovich. "Implications of Temperature and Buffering Systems for Laboratory Testing of Alloy Steel and 13Cr Materials in Oil and Gas Production Environments." In CORROSION 2011. NACE International, 2011. https://doi.org/10.5006/c2011-11096.
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Abstract This paper describes the results of a laboratory study evaluating cracking resistance of 4130 (UNS G41300), 13Cr-L80 (UNS S42000), and two modified “13-5-2” type 13Cr alloys (UNS S41426) with 110 ksi (758 MPa) specified minimum yield strength in three different oil and gas well environments. Sulfide stress cracking resistance was evaluated using tensile specimens stressed to 90% actual yield strength and double cantilever beam specimens. Three environments were evaluated that included: (a) NACE Solution A with 15 psia (0.1 MPa) H2S; (b) a simulated oil well with 100,000 mg/L Cl−, pH 4.5, 0.5 psia (3.5 kPa) H2S; and (c) a simulated gas well with 1,000 mg/L Cl−, pH 3.5, 0.5 psia (3.5 kPa) H2S. These three environments were used for tests at both room temperature and at 40 °F (5 °C). Also, the oil well and gas well simulated environments were tested using both an acetate and bicarbonate buffer solution for pH control. Cracking and corrosion observations are reviewed and implications of alloy sour service limits, effect of temperature, and effect of buffering agent in laboratory testing are discussed. Findings of the current study are compared with previously presented studies to confirm or challenge assumptions on the role of temperature and buffering systems.
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Ritter, S., and H. P. Seifert. "Stress Corrosion Cracking Behavior of Low-Alloy Reactor Pressure Vessel Steels and of a Weld Filler Material under Simulated BWR Environment." In CORROSION 2003. NACE International, 2003. https://doi.org/10.5006/c2003-03664.
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Abstract The stress corrosion cracking (SCC) behavior of three different nuclear grade reactor pressure vessel (RPV) steels (SA 533 B Cl.1, SA 508 Cl.2, 20 MnMoNi 5 5) and of a RPV weld filler material was characterized under simulated boiling water reactor (BWR)/normal water chemistry (NWC) conditions by constant and ripple load tests with pre-cracked fracture mechanics specimens. The experiments were performed in oxygenated high-temperature water at temperatures of either 288, 250, 200 or 150 °C. Modern high-temperature water loops, on-line crack growth monitoring (DCPD) and fractographical analysis by SEM were used to quantify the cracking response. It was concluded that there is no susceptibility to sustained SCC crack growth under purely static loading in oxygenated high-temperature water (ECP ≤ 150 mVSHE) at 288 °C for stress intensity factors KI ≤ 60 MPa·m1/2 if the water chemistry is maintained within current BWR/NWC operational practice (EPRI water chemistry guidelines). However, sustained, fast SCC cannot be excluded for faulted water chemistry conditions and/or for highly stressed specimens, either loaded near to KIJ or with a high degree of plasticity in the remaining ligament. The conservative character of the “BWR VIP 60 SCC disposition lines 1 and 2” for SCC crack growth in low-alloy steels (LAS) has been confirmed by this study for 288 °C and RPV base and weld filler material. Preliminary results indicate that these disposition lines may be significantly exceeded in the case of small load fluctuations at high load ratios (ripple loading) or at intermediate temperatures (200 – 250 °C) in RPV materials, which show a distinct susceptibility to dynamic strain aging (DSA). The concentration of “free” interstitial nitrogen/carbon might therefore be just as relevant for SCC susceptibility as the steel sulfur content or the morphology, size and distribution of the MnS-inclusions, at least under conditions where DSA is typically observed.
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Mansfeld, F., and Y. Wang. "Corrosion Protection of High-Copper Aluminum Alloys Using Green Technology." In CORROSION 1995. NACE International, 1995. https://doi.org/10.5006/c1995-95041.
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Abstract The concept of surface modification as a new method of corrosion protection using chemicals without toxic problems is described for the Al alloys Al 6061, Al 7075-T6 and Al 2024-T3. In the Ce-Mo process Ce and Mo are incorporated into the original oxide film by chemical and electrochemical processes. The resulting surfaces are resistant to pitting in aggressive solutions such as 0.5 N NaCl. Surface modified Al 6013 has passed the salt spray test according to ASTM B 117. For Al 6061 and 7075, hot solutions of CeCl3 and Ce(NO3)3 are used, while for Al 2024 CeCl3 is replaced by Ce acetate. For all alloys anodic polarization is carried out in Na2MoO4. For Al 2024 and Al 7075 a Cu removal pre-treatment step is used in which Cu intermetallic compounds are removed from the outer surface layers. The resistance to localized corrosion has been evaluated by recording of impedance spectra in 0.5 N NaCl for 30 days. Surface analysis data suggest that Ce and Mo are concentrated at sites where local cathodes such as Cu intermetallic compounds are located. Polarization curves show that both the cathodic and the anodic reaction are inhibited on modified surfaces. The pitting potential Epit is increased for surface modified samples at constant corrosion potential Ecorr. This result could be due to a decrease of the amount of Cl− adsorbed at a given potential for oxide layers containing Ce and Mo.
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Efird, K. D., E. J. Wright, J. A. Boros, and T. G. Hailey. "Experimental Correlation of Steel Corrosion in Pipe Flow with Jet Impingement and Rotating Cylinder Laboratory Tests." In CORROSION 1993. NACE International, 1993. https://doi.org/10.5006/c1993-93081.
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Abstract The results from the first phase of research to quantify the relationship of laboratory fluid flow corrosion test techniques to field applications and the parameters required to effectively apply laboratory data to plant operations are presented. Single phase, aqueous, sweet corrosion of steel in turbulent pipe flow (12.7 and 25.4 mm diameter) is correlated to corrosion in jet impingement and rotating cylinder tests. All tests were simultaneously conducted using the same test fluid (3.0% NaCl + 1000 ppm HCO3− solution at pH 6.0 with 20-30 ppb O2 and 1.3 bar (20 psia) CO2 at 50°C) to minimize environmental variables and allow a realistic comparison of test methods. The results demonstrate that, for this environment, the rotating cylinder electrode corrosion rates do not correlate with pipe flow based on the commonly accepted wall shear stress, while jet impingement corrosion rates at r/ro=3 do correlate. The general equation for flow induced carbon steel corrosion in this environment is: RCOR=aτwb,where "RCOR" is the carbon steel corrosion rate in mm/y and "τw" is the wall shear stress in N/m2. For the environment tested, the coefficient "a" is 12.5 ± 0.5, "b" is 0.10 ± 0.02. The effect of solution chemistry (PCO2, pH, Fe++, HCO3–, Cl–, etc.) is contained in the equation coefficient and exponent, and requires further experimental definition. The fluid parameters (ρ, μ, e, etc.) are included in the wall shear stress. The generally accepted wall shear stress calculation for the rotating cylinder is apparently incorrect when applied to the effect on corrosion. The equation for rotating cylinder wall shear stress that correlates the rotating cylinder corrosion rate with pipe flow corrosion rate is expressed as: τw=1.8×10−8ϖ1.7,where "τw" is the wall shear stress in N/m2 and “ϖ” is the rotation speed in rad/s. The electrochemical impedance data indicate the corrosion of carbon steel is under charge transfer control in this environment and the increase in corrosion rate with shear stress is related to a decrease in charge transfer resistance in all three fluid flow methods.
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Andrianopoulou, S., M. Schmitt, V. Grüßinger, B. Lippert, and U. Martens. "Simultanes kutanes Plattenepithelkarzinom und B-CLL: Grenzen innovativer Therapiekonzepte." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685815.
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Deng, Jiusheng, Jonathon Cohen, Andrea Pennati, et al. "Abstract A11: GIFT4-reprogrammed leukemic B cells for CLL immunotherapy." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-a11.
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Davis, Joanne, Kylie Mason, Chia Sharpe, et al. "Abstract B054: Can CLL-B cells treated with novel combination therapies be used to promote anti-CLL immune responses?" In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b054.
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Al Sharifi, Liqaa, Haider Abdul Ridha, Ahmed Rashid, Sinan Muhsin, and Teeb Jaafer. "Role of CD200 and CD43 in Diagnosis and Prognosis of CLL and NHL Patients." In 5th International Conference on Biomedical and Health Sciences. Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/biohs2024/paper.1403.
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Background: Chronic lymphoproliferative disorder (LPD), is a malignant disease of lymphocytes in the blood and lymphatic tissue. Chronic lymphocytic leukaemia, it is the commonest type of chronic lymphoproliferative disorder. Scoring by immunophenotyping is used to differentiate B-cell chronic lymphocytic leukemia from other B-Non-Hodgkin lymphomas. CD200 (OX2) is a glycoprotein of membrane, it is related to type I superfamily of immunoglobulin . CD43 (Sialophorin) is a sialoglycoprotein that is present on the surface of T lymphocytes, some B lymphocytes, granulocytes and monocytes, that play important role for immune function and also play a role as physiologic ligand-receptor complex involved in T- cell activation. Aim of study-Evaluate the role of CD200 and CD43 positive expression and co-expression in diagnosis and prognosis of CLL and NHL. Subjects and Methods: This cross sectional study on one hundred forty five patients with chronic lymphoprliferative disorders who were attending Baghdad teaching hospital at medical city from beginning of January 2020 to end of December 2020, patients divided in to two groups; chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma (NHL) patients At diagnosis, there was assessment of CD200 and CD43. Clinical and laboratory data were done including staging by modified Rai, and Ann arbor staging system ( for CLL and NHL respectively), then follow up for about 6-12. Results: There is significant statistical correlation between CD 200 and CD 43 and often co-expression of both in differentiation between CLL and NHL (p value < 0.001). Almost all patients of CD 200 positive expression show moderate to bright pattern of expression in CLL in apposite to NHL patients, who showed dim to moderate pattern of expression, while the great majority of CD43 expression was dim to moderate pattern in both CLL and NHL patients.In CLL patients there was no significant correlation between prognostic markers (age, Hb, platelets count, lymphocytes count and CD 38 expression) and CD200, CD 43. For NHL patients, all markers show no significant correlation except that CD 43 show significant correlation with expression of CD 38. Conclusion: CD200, CD43 and often co-expression of both have a significant value in diagnosis and differentiation of CLL from B- NHLs.
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Santanam, Urmila, Nicola Zanesi, Alexey Efanov, et al. "Abstract LB-352: B-CLL phenotype in Eµ-miR-29 transgenic mice." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-352.
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Lai, Hsien, Suping Zhang, Christina Wu, et al. "Abstract 950: Selective cytotoxicity of A6 peptide against ZAP-70 expressing CLL B-cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-950.
Full textReports on the topic "B-CLL"
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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test MIL-M-9977J. Appendix J. NATO Stage B Cross-Servicing Checklist (CL2) Document Type Definition. Defense Technical Information Center, 1994. http://dx.doi.org/10.21236/ada306309.
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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test MIL-M-9977J. Appendix I. NATO Stage B Cross-Servicing Checklist (CL1) Document Type Definition. Defense Technical Information Center, 1994. http://dx.doi.org/10.21236/ada306310.
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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test, MIL-M-9977J, Appendix J, NATO Stage B Cross-Servicing Checklist (CL2), Document Type Definition. Defense Technical Information Center, 1994. http://dx.doi.org/10.21236/ada309304.
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Reid, M. S., X. Wang, N. Utting, and C. Jiang. Comparison of water chemistry of hydraulic-fracturing flowback water from two geological locations at the Duvernay Formation, Alberta, Canada. Natural Resources Canada/CMSS/Information Management, 2021. http://dx.doi.org/10.4095/329276.
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We analyzed and compared the water chemistry between 17 Fox Creek region samples, each from a different well, and 23 Three Hills region samples from a single well. Overall, the two regions were similar in chemical composition but showed small differences in some lower abundance dissolved elements. Additionally, we investigated changes in water chemistry of FPW over time from a single well. The majority of water quality parameters and water chemistry remained constant over the 7-month sampling time. Major ion chemistry showed increasing concentrations of Ca and Mg, and a decreasing concentration of SO4. Several trace elements also showed small trends of both increasing and decreasing concentrations over time. There was a strong correlation between Ca and Mg concentrations in both the Fox Creek region samples and Three Hills region samples, which is an indication of the mixing of formation water. However, the correlation between B and Sr was different among two region samples, which is likely due to the delayed mixing of formation water with the fracturing fluids during the flowback at different time periods of post fracturing. Likewise, Fox Creek region samples showed correlations between concentrations of Cl and Ca, Na and Ca, and Na and Mg, but these correlations were not seen in the Three Hills region samples. Geochemical modeling demonstrates that there are potential scales formed in the flowback water, but most of the minerals are still in the dissolution state in the formation. Stable isotopic analysis confirmed the mixing of injection water and the formation water.
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Jauvin, Nathalie, François Aubry, Francis Ethridge, et al. Recherche-action visant le développement d’un modèle d’intervention préventive en SST par et pour les préposés aux bénéficiaires en CHSLD. IRSST, 2024. http://dx.doi.org/10.70010/nkup8051.
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Contexte Ce rapport a pour objectif de présenter les résultats d’une recherche-action visant le développement d’un modèle d’intervention préventive en santé et sécurité du travail (SST) par et pour les préposés aux bénéficiaires (PAB) dans les centres d’hébergement et de soins de longue durée (CHSLD) du Québec. Les PAB sont au cœur des soins prodigués dans les milieux gériatriques. Malheureusement, l’augmentation du nombre de blessures et l’accentuation des problématiques de santé psychologique subies par ce personnel depuis quelques années fragilisent leur situation, ce qui se prouve en termes de faible rétention et de fort absentéisme chronique de ce personnel. Ce projet, qui est issu au départ d’une demande du milieu, visait à implanter une démarche d’intervention dans trois CHSLD du Québec, en nous inspirant d’autres études menées dans d’autres types d’organisation, comme les centres jeunesse. Revue de littérature La littérature scientifique nous enseigne que la participation des travailleurs au développement et à l’implantation de programme de prévention de la SST est une condition clé de leur succès, et ce préférablement à une intervention unilatéralement « classique » davantage axée uniquement sur la formation du personnel. Néanmoins, les CHSLD ne sont pas reconnus comme des milieux innovants, dans lesquels les PAB peuvent participer activement au développement des programmes de formation qui les concerne. La participation des PAB à une intervention préventive en SST, même si elle leur est destinée, apparaît comme un défi particulièrement important et difficile à relever. Objectifs L’objectif principal de cette recherche-action consistait à développer des modalités d’interventions préventives innovantes en matière de SST portées principalement par les PAB en CHSLD, afin d’en tirer des connaissances généralisables à d’autres milieux. Nos objectifs spécifiques visaient à : 1) cerner, dans les CHSLD, les facteurs de risque ainsi que les facteurs de protection présents ; 2) documenter et évaluer un processus mené « pour et par des PAB » qui vise à réduire les contraintes ciblées dans chaque milieu ; 3) documenter et évaluer le processus d’implantation de ces mesures ainsi que la participation des PAB dans la mise en place de la démarche ; 4) documenter les effets attendus des interventions proposées au sein des groupes de soutien à l’intervention (GSI) ; 5) dresser un inventaire des conditions (dimensions contextuelles et organisationnelles) favorables ou défavorables à l’implantation d’une intervention préventive misant sur la participation des préposés aux bénéficiaires. Cadre d’intervention L’étude a pris la forme d’une recherche-action. Selon cette approche, c’est principalement par l’action que l’on peut générer des connaissances scientifiques pour comprendre et changer la réalité sociale des individus et des systèmes, donc d’organisations telles que les CHSLD. Dans cette perspective, la théorie découle donc de l’action. Dans le cadre d’une recherche-action, on vise notamment à garantir que l’objet réponde à la fois aux problèmes pratiques des membres de l’organisation ainsi qu’aux préoccupations théoriques de recherche. Aussi, nous nous sommes appuyé sur le cadre proposé par Goldenhar et al., (2001) pour élaborer la démarche d’intervention. Il s’agit d’un modèle en 3 phases : le développement (l’identification a priori des risques ciblant des priorités sur lesquelles agir), l’implantation (l’implantation d’une intervention cohérente avec ces cibles via un GSI) et l’évaluation de l’intervention (l’étude de l’efficacité de l’intervention). Méthodologie Notre processus méthodologique a suivi le cadre d’intervention précité, soit trois phases de recherche-action : le diagnostic (phase I), l’intervention (phase II) et l’évaluation (phase III), et ce, dans trois CHSLD différents. Mentionnons que nous avons rajouté une phase d’entrevues, à la suite de la pandémie de la COVID-19 (phase I-B). Nous avons réalisé un total de 50 entrevues, soit 36 lors de la phase I (trois sites) et 21 en phase I-B. Nous avons réalisé également des heures d’intervention dans le cadre de la phase II, afin de développer les GSI. Lors des phases II et III, 15 informateurs clés ont été rencontrés sur une base individuelle et volontaire, et ce dans les deux CHSLD où ont été implantés des GSI. Notons que la pandémie a considérablement freiné notre projet et limité la portée de notre action. Il a été décidé, à la suite de la phase I-B, qu’un CHSLD serait supprimé de notre projet, tant les enjeux de recrutement pour les entrevues (phase I-B) et GSI (phase II) semblaient complexes. Résultats Les résultats de la phase I et I-B mettent de l’avant, dans les trois milieux, des facteurs de risque et des facteurs de protection relatifs à la charge de travail, au manque de soutien des collègues ou des supérieurs, à la faible reconnaissance et à la faible autonomie décisionnelle. Ce diagnostic a permis de préciser certaines pistes d’action pour les deux CHSLD participant à la phase II. Nous présentons ces pistes, de même que le processus complexe par lequel nous avons pu (ou non) développer des innovations organisationnelles dans les milieux. Dans le CHSLD du Hameau, quatre mesures ont été retenues (p. ex. : procéder à un exercice de clarification des rôles, des tâches partagées). Au CHSLD du Parvis, quatre mesures ont été aussi retenues (p. ex. élaborer un plan de contingence sur les unités). En guise d’évaluation, nous présentons plusieurs conditions gagnantes et défis identifiés par les acteurs des milieux interrogés. Discussion Notre projet a permis de documenter la complexité de développer des projets participatifs en CHSLD, notamment lorsqu’ils visent les PAB. Un premier facteur de complexité porte sur la structure hiérarchique même de l’organisation, qui donne peu de place et de pouvoir aux PAB, alors même que cette catégorie d’emploi est centrale en CHSLD. Un second facteur a trait à la fragilité importante de ces processus d’innovations lorsque des contraintes extérieures entravent ou bouleversent les pratiques quotidiennes. Certaines contraintes peuvent être importantes et de courte durée (comme la pandémie de la COVID-19), mais d’autres sont relativement récurrentes et fragilisent tout autant le même processus (manque de main-d’œuvre ponctuelle, épidémie d’influenza, visites de qualité, etc.). Des facteurs de soutien sont identifiés, comme l’engagement structuré de l’ensemble de l’organisation envers le projet (des hautes directions comme SAPA aux gestionnaires immédiats), la composition rigoureuse du comité chargé de développer et d’implanter les mesures proposées et le développement d’une perspective de pérennisation à moyen et long terme.
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Guy, Charles, Gozal Ben-Hayyim, Gloria Moore, Doron Holland, and Yuval Eshdat. Common Mechanisms of Response to the Stresses of High Salinity and Low Temperature and Genetic Mapping of Stress Tolerance Loci in Citrus. United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7613013.bard.
Full textAbstract:
The objectives that were outlined in our original proposal have largely been achieved or will be so by the end of the project in February 1995 with one exception; that of mapping cold tolerance loci based on the segregation of tolerance in the BC1 progeny population. Briefly, our goals were to 1) construct a densely populated linkage map of the citrus genome: 2) map loci important in cold and/or salt stress tolerance; and 3) characterize the expression of genes responsive to cold land salt stress. As can be seen by the preceding listing of accomplishments, our original objectives A and B have been realized, objective C has been partially tested, objective D has been completed, and work on objectives E and F will be completed by the end of 1995. Although we have yet to map any loci that contribute to an ability of citrus to maintain growth when irrigated with saline water, our very encouraging results from the 1993 experiment provides us with considerable hope that 1994's much more comprehensive and better controlled experiment will yield the desired results once the data has been fully analyzed. Part of our optimism derives from the findings that loci for growth are closely linked with loci associated with foliar Cl- and Na+ accumulation patterns under non-salinization conditions. In the 1994 experiment, if ion exclusion or sequestration traits are segregating in the population, the experimental design will permit their resolution. Our fortunes with respect to cold tolerance is another situation. In three attempts to quantitatively characterize cold tolerance as an LT50, the results have been too variable and the incremental differences between sensitive and tolerant too small to use for mapping. To adequately determine the LT50 requires many plants, many more than we have been able to generate in the time and space available by making cuttings from small greenhouse-grown stock plants. As it has turned out, with citrus, to prepare enough plants needed to be successful in this objective would have required extensive facilities for both growing and testing hardiness which simply were not available at University of Florida. The large populations necessary to overcome the variability we encountered was unanticipated and unforeseeable at the project's outset. In spite of the setbacks, this project, when it is finally complete will be exceedingly successful. Listing of Accomplishments During the funded interval we have accomplished the following objectives: Developed a reasonably high density linkage map for citrus - mapped the loci for two cold responsive genes that were cloned from Poncirus - mapped the loci for csa, the salt responsive gene for glutathione peroxidase, and ccr a circadian rhythm gene from citrus - identified loci that confer parental derived specific DNA methylation patterns in the Citrus X Poncirus cross - mapped 5 loci that determine shoot vigor - mapped 2 loci that influence leaf Na+ accumulation patterns under non-saline conditions in the BC1 population - mapped 3 loci that influence leaf Na+ accumulation paterns during salt sress - mapped 2 loci that control leaf Cl- accumulation patterns under non-saline conditions - mapped a locus that controls leaf Cl- accumulation patterns during salt stress Screened the BC1 population for growth reduction during salinization (controls and salinized), and cold tolerance - determined population variation for shoot/root ratio of Na+ and Cl- - determined levels for 12 inorganic nutrient elements in an effort to examine the influence of salinization on ion content with emphasis on foliar responses - collected data on ion distribution to reveal patterns of exclusion/sequestration/ accumulation - analyzed relationships between ion content and growth Characterization of gene expression in response to salt or cold stress - cloned the gene for the salt responsive protein csa, identified it as glutathione peroxidase, determined the potential target substrate from enzymatic studies - cloned two other genes responsive to salt stress, one for the citrus homologue of a Lea5, and the other for an "oleosin" like gene - cold regulated (cor) genes belonging to five hybridization classes were isolated from Poncirus, two belonged to the group 2 Lea superfamily of stress proteins, the others show no significant homology to other known sequences - the expression of csa during cold acclimation was examined, and the expression of some of the cor genes were examined in response to salt stress - the influence of salinization on cold tolerance has been examined with seedling populations - conducted protein blot studies for expression of cold stress proteins during salt stress and vice versa