14 research outputs found
Correlation between delay in treatment initiation and disease severity scores.
No full textDelay in initiation of treatment for GD (ΔTX) was plotted against disease severity score (DS3) for each patient. The trend line shows a positive Pearson correlation coefficient between the two values (r value = 0.55, P = 0.0018) (A). Subjects were divided based on their DS3 scores as being mild/moderate (DS36) and their ΔTX values were plotted. Unpaired Student’s t-test revealed P value = 0.0036 (**) indicating very significant difference (B).</p
Demographic and clinical data from 31 GD patients enrolled into IRB approved study.
No full textDemographic and clinical data from 31 GD patients enrolled into IRB approved study.</p
Inflammatory cytokine expression on T cells.
No full textMemory T cells were further analyzed for co-expression of inflammatory chemokine receptors (CCR4, CCR5 and CCR6) which play a role in T cell mediated inflammation.</p
Activation markers in Th and Tc cells.
No full textCD4+ T (A) and CD8+ T cells (B) were further analyzed for expression of activation markers (CCR4, CXCR3), chemokine receptor (CCR6) and chemoattractant (CRTH2) which play a role in T-cell mediated inflammation.</p
Effect of early or delayed therapy on immune irregularities.
No full textGD patients were sub-divided into those who received early vs. delayed intervention after their diagnosis and plotted for specific immune phenotypes. B cell transitional cells expressed as CD21Dim (A), IgA producing B cells (B), NKT cells (C) and dendritic cell (D) percentages in GD patients with delayed or early intervention are plotted.</p
Correlation between immune alterations and ΔTX, DS3 and combined scores.
No full textGD patients were sub-categorized based on whether or not they show persistent B-cell (A), T-cell (B), NKT cells (CD16/CD56+ T cells) (C) and dendritic cell (D) immune alterations and plotted against the delay in initiation of ERT (ΔTX), disease severity (DS3) and a combined score (ΔTX+DS3).</p
NK/NKT and dendritic cells in GD patients.
No full textNK cells (CD3-/ CD16+ or CD56+), NKT cells (CD3+/ CD16+ or CD56+) and invariant NKT cells (iNKT, CD3+, Vα24Jα18+, CD4+/CD8+) from peripheral blood of GD patients and normal controls were assessed using flow cytometry and plotted as percentage of total lymphocytes (A-D). Dendritic cells were enumerated as Lin-/CD34-/HLA DR+ cells and plotted as a percentage of total leukocytes/WBCs (E). Dendritic cells were further fractionated as myeloid DCs or plasmacytoid DCs based on expression of CD11c and BDCA2 respectively and plotted as percentage of DCs (F&G).</p
T-lymphocytes and subsets in GD patients.
No full textT-lymphocytes (CD3+) from peripheral blood of GD patients and normal controls were assessed using flow cytometry and plotted as fraction of total lymphocytes (A). T helper cells (CD3+/CD4+) (B) and cytotoxic T cells (CD3+/CD8+) (C) were calculated and a ratio of CD4 to CD8 cells was plotted (D). Similarly memory subsets of CD4 (CD3+/CD4+/CD45RO+) and CD8 T cells (CD3+/CD8+/CD45RO+) were calculated and plotted against normal controls (E, F). Unpaired student’s t-test was performed to calculate significance values and included in the plots where significant difference between GD and normal controls was observed.</p
Measurement of the Gamma (b anti-b) / Gamma (hadron) branching ratio of the Z by double hemisphere tagging
No full textTwo measurements of {Mathematical expression} are presented. Both measurements use 250000 Z decays taken with the DELPHI detector in 1991 and rely mainly on the precision of the microvertex detector. One tagging method is as simple as possible so that background rates can be reliably predicted by simulation. The other one uses a more involved tagging technique and reduces the dependence on simulation as much as possible. Combining both results, {Mathematical expression} is found to be 0.2209±0.0041(stat.)±0.0042(syst.)±0.0018 {Mathematical expression}. © 1995 Springer-Verlag.0SCOPUS: ar.jinfo:eu-repo/semantics/publishe
