Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of interleukin-1 (IL-1) was examined in cultured CNS microglia obtained from trisomy 16 (Ts16) fetal mouse brain, a model system for studies relevant to Down syndrome (DS). When compared to microglia from their normal littermates, Ts16 microglia produced significantly higher levels of IL-1 activity both before and following stimulation with lipopolysaccharide (LPS). IL-1 release was stimulated by alpha/beta interferon (IFN) in the normal but not Ts16 microglial cultures. The overall level of IL-1 production in normal littermates, however, was still less than that seen in Ts16. Thus, microglia from Ts16 mice may function in an inappropriate manner and, if this abnormality occurs in vivo, may have wide ranging effects on a developing nervous system.
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PMID:Abnormal production of interleukin-1 by microglia from trisomy 16 mice. 172 92

The results of cytogenetic studies are reported in 89 patients with B-cell CLL. LPS (E. coli lipopolysaccharide), PWM (pokeweed mitogen), PHA (phytohaemagglutinin), EBV (Epstein-Barr virus), TPA (phorbol 12-myristate 13-acetate), and LA (leucoagglutinin) were used as mitogens. Mitoses were obtained from 78 cases. Clonal aberrations could be demonstrated in 26 cases. Trisomy 12 was the most frequent finding (8 cases) and was sole abnormality in 4 cases. Chromosomes #14, #17, and #11 were involved in structural aberrations in 5, 7, and 7 cases respectively, but a t(11;14)(q13;q32) was the only structural aberration seen more than once. The median observation time was 47 months (range 1-87). The presence of clonal abnormalities did not influence survival significantly, either when calculated from diagnosis or from cytogenetic analysis. Patients with more than one aberration, however, had a significantly shorter survival than patients with normal mitoses only (p less than 0.05). The survival of 8 patients with trisomy 12 (in 4 as sole abnormality) was not different from that of patients with normal mitoses only.
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PMID:B-cell chronic lymphocytic leukaemia: clonal chromosome abnormalities and prognosis in 89 cases. 261 12

The chromosomal constitution of stimulated lymphocytes in 13 patients with B cell chronic lymphocytic leukemia (B-CLL) were sequentially examined using polyclonal B cell activators (PBA), i.e., Epstein-Barr virus (EBV), lipopolysaccharide W from E. coli (LPS), pokeweed mitogen (PWM), and protein A from Staphylococcus aureus (PA). Of the 11 patients (44 samplings) with abnormal clones, 2 patients had only trisomy 12, 6 patients had trisomy 12 plus other clonal abnormalities, such as +8, +9, +16, +18, 6q-, 15q+, and t(4;15), and the remaining 3 cases had various clonal abnormalities other than trisomy 12, such as trisomy 3, 8, 20, 21, and insertion of #7 and #12. These findings suggest that even though trisomy 12 may be a common abnormality in B-CLL, various other abnormal clones may also be present in vivo for relatively long periods of time. It appears that stimulated lymphocytes in patients with previous therapy tend to show chromosome abnormalities more frequently than those in untreated patients.
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PMID:Sequential chromosome abnormalities in B cell chronic lymphocytic leukemia: a study of 13 cases. 348 71

The characterisation of a new murine B cell lymphoma, A31, is described. Histopathological examination of passaged tumour indicates that initial infiltration occurs in the spleen, lymph nodes, Peyer's patches and liver, while in the terminal phase the bone marrow, gonads and occasionally the central nervous system become involved. The terminal spread is coincidental with the leukaemic phase in the tumour. The tumour cells show typical B cell characteristics in vitro. These include surface immunoglobulin (Ig) of mu, kappa isotype, surface Ia, Thy-1 negativity and an increased uptake of tritiated thymidine following incubation with lipopolysaccharide. A31 cells secrete low levels of IgM into the tissue culture fluid. Short-term culture produced only 100 ng IgM per 10(7) cells over 8 h and no tumour-associated monoclonal band could be detected in the serum of tumour-bearing mice. Chromosomal karyotypes of A31 cells gave model numbers 2n=40 normal, and 2n=41, with partial trisomy of chromosome 2, and trisomy of 17. There was loss of a chromosome 6 and the Y chromosome, together with the translocation of part of an 11 to one of the two unidentified marker chromosomes. The responses of lymphoma-bearing mice to therapeutic levels of cyclophosphamide and vincristine sulphate and also to whole body X-radiation are illustrated. This tumour may help in unravelling the complex biology of B cell lymphoma and because of its low level of Ig secretion, be of particular value in experimental immunotherapy.
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PMID:Characterisation of a new murine B cell lymphoma. 349 18

The chromosomes of stimulated lymphocytes in 40 treated cases of B-cell chronic lymphocytic leukemia (B-CLL) were examined. The polyclonal B-cell activators (PBA) used were: pokeweed mitogen (PWM), Epstein-Barr virus (EBV), and lipopolysaccharide W from Escherichia coli 055:B5 (LPS). Thirty-three (83%) of the 40 cases contained an adequate number of metaphases that were suitable for banding. Of 15 cases with abnormal clones, 7 cases had trisomy #12. Occasionally, trisomy #1, 6q-, i(7q), 14q+, trisomy #16, and trisomy #18 were seen. In 5 cases, marker chromosomes of unknown origin existed. The findings indicate that trisomy #12 may be a unique and nonrandom karyotypic change in B-CLL.
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PMID:Chromosomes and causation of human cancer and leukemia. LII. Chromosome findings in treated patients with B-cell chronic lymphocytic leukemia. 631 64

Lymphocytes from 33 out of 63 patients with B-cell chronic lymphocytic leukaemia (B-CLL) were successfully stimulated for cytogenetic analysis by means of two B-cell mitogens: pokeweed mitogen and lipopolysaccharide-B, used after pretreatment of the cells with neuraminidase and galactose oxidase. All patients had abnormal clones in 30-100% of the cells analysed. Chromosomes more frequently involved were Nos. 1, 3, 6, 11, 12, 13 and 14. The most common abnormality was a marker 14q+ (breakpoint 14q32) seen in 17 cases; trisomy 12 was observed in seven cases. A clinical scoring system was used to investigate the correlation of chromosome abnormalities with prognosis. The group with 14q+ was often associated with features of progressive disease, namely; prolymphocytoid or Richter transformation, refractoriness to therapy, high WBC and advanced staging. A significant difference in survival was observed between patients with 14q+ and the rest: median survival from diagnosis being 45 months and over 64 months, respectively (P less than 0.05); when survival was calculated from the time of chromosome analysis the values were 8 months and more than 41 months, respectively (P less than 0.01). It is suggested that 14q+ is acquired during the evolution of CLL and that this development may be a key event in the clinical progression of B-CLL. Other abnormalities, including trisomy 12, were not found to be associated with a worse prognosis.
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PMID:Prognostic significance of chromosome abnormalities in chronic lymphocytic leukaemia. 633 48

The chromosome constitutions of stimulated lymphocytes in 21 untreated cases with B-cell chronic lymphocytic leukemia (B-CLL) were examined. So-called polyclonal B-cell activators, i.e., pokeweed mitogen, Epstein-Barr virus, and lipopolysaccharide W from E. coli 055:B5, were used. Four out of 21 cases showed abnormal clones with trisomy 12 and were started on therapy shortly after the diagnosis and cytogenetic examination. On the other hand, most cases without abnormal clones had not received treatment for relatively long periods before and after cytogenetic examination. These findings may indicate that cytogenetic results can be utilized as a parameter for treatment and prognosis in B-CLL.
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PMID:Clinical significance of cytogenetic findings in untreated patients with B-cell chronic lymphocytic leukemia. 660 86

Using a sister chromatid differentiation technique, cell cycle study of stimulated lymphocytes of B-cell chronic lymphocytic leukemia (B-CLL) revealed their cell cycle progression to be similar to that of normal lymphocytes stimulated by T-cell and various polyclonal B-cell activators (PBA). The chromosome constitutions of stimulated lymphocytes in 62 patients with B-CLL were examined using PBA such as Epstein-Barr virus (EBV) and lipopolysaccharide W from E. coli 055:B5 (LPS). Of the 20 patients with abnormal clones, 11 patients had trisomy 12; other less common abnormalities were trisomy 1, 6q-, i(7q), 14q+, trisomy 16, trisomy 18, reciprocal translocations, and marker chromosomes of unknown origin. These findings indicate that trisomy 12 may be a unique and common karyotypic change in B-CLL. The fact that 3 out of 4 patients with marker chromosomes showed stage IV disease may indicate that a clone with a marker is a predictor of an unfavourable prognosis. The near correlation between trisomy 12 and kappa chains existed (0.05 less than p less than 0.10). Trisomy 12 was seen in all 5 patients with monoclonal paraprotein.
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PMID:Chromosome studies in stimulated lymphocytes of B-cell chronic lymphocytic leukemias. 661 Jun 24

Superoxide dismutases (SODs) scavenge superoxide anion and participate in an essential role as a defense system against oxidative stress in body. Cu,Zn-SOD is localized at cytoplasm. A defect in the Cu,Zn-SOD gene has been demonstrated in some cases of familial amyotrophic lateral sclerosis. Trisomy of chromosome 21 in Down's syndrome increases the level of this isozyme and causes the disease. Inactivation of Cu,Zn-SOD by glycation under hyperglycemic conditions may also be a critical factor for diabetic complication. The expression of the second isozyme, Mn-SOD localized at mitochondrial matrix, is regulated in a complex manner by many stimulants such as interleukin-1, -6, tumor necrosis factor, lipopolysaccharide, and tumor promoters phorbol ester (TPA) and okadaic acid. This isozyme seems to work as a defense mechanism against damage during inflammatory responses. The third isozyme, extracellular SOD, is highly glycosylated and has affinity for heparin sulfate. This may participate in scavenging superoxide in plasma and, therefore, missense mutation in heparin binding domain increases the serum level of this isozyme, although the physiological role is not clearly understood yet.
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PMID:[Physiological significance of superoxide dismutase isozymes]. 760 83

The results of cytogenetic studies are reported in 76 patients with B-chronic lymphoproliferative disorders (B-CLPD): 60 patients with chronic lymphocytic leukemia (CLL), six with follicular lymphoma in leukemic phase (FLLP), five with splenic B-cell lymphoma with villous lymphocytes (SLVL), two with chronic prolymphocytic leukemia (CPL), two with hairy cell leukemia (HCL), and one with plasma cell leukemia (PCL). PHA (phytohemagglutinin), PWM (pokeweed mitogen), LPS (lipopolysaccharide from Escherichia Coli), TPA (phorbol 12-myristate acetate), IL6 (interleukin 6), and DxS (dextran sulfate) were used as mitogens. Mitoses were obtained in 75 cases. Clonal aberrations could be demonstrated in 34 cases (44%). In CLL, classical type, chromosomes 6, 11, and 13 were more frequently involved, whereas trisomy 12 was frequently found in CLL mixed-cell type, in FLLP, and CPL. In SLVL the deletion del(7)(q32) is noteworthy and miscellaneous chromosome abnormalities in the remaining patients were observed. Regarding the efficiency of mitogens, PHA turned to be the most effective in obtaining metaphases and in detecting clonal chromosomal aberrations.
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PMID:Cytogenetic studies in seventy-six cases of B-chronic lymphoproliferative disorders. 907 2


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