691 research outputs found
The time-dependent localization of Ki 67 antigen-positive cells in human skin wounds
A total of 77 human skin wounds with a post-infliction interval between 3 h and 7 months were investigated and the proliferation marker antigen Ki 67 was visualized in paraffin sections using a specific monoclonal antibody (MIB). The re-built epidermal layer covering the former lesional area showed only a few basal cells positively staining for Ki 67 antigen. No enhanced reactivity was found when compared to uninjured skin. In basal cells of the epidermis adjacent to the wound area, however, varying numbers of positive cells occurred, but no information useful for a reliable time estimation of skin wounds could be obtained due to the considerable variability in the number of Ki 67 positive epidermal basal cells found in non-damaged skin. Fibroblastic cells in the wound area revealed an increased number of Ki 67-positive sites which could first be detected in a 1.5-day-old skin lesion. Positive results could be obtained in every specimen investigated after a post-infliction interval of 6 days up to 1.5 months. Only the scar tissue of the oldest wound examined (wound age 7 months) revealed no increase in the number of positively staining fibroblasts. Therefore, positive results indicate a wound age of at least approximately 1.5 days and the lack of an increased number of positive fibroblastic cells in a sufficient number of specimens indicates at a wound age of less than 6 days, but cannot totally exclude longer post-infliction intervals
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Localisation of the Ki-67 antigen within the nucleolus: Evidence for a fibrillarin-deficient region of the dense fibrillar component
The Ki-67 antigen is detected in proliferating cells in all
phases of the cell division cycle. Throughout most of interphase,
the Ki-67 antigen is localised within the nucleolus.
To learn more about the relationship between the Ki-67
antigen and the nucleolus, we have compared the distribution
of Ki-67 antibodies with that of a panel of antibodies
reacting with nucleolar components by confocal laser
scanning microscopy of normal human dermal fibroblasts
in interphase stained in a double indirect immunofluorescence
assay. During early G1, the Ki-67 antigen is
detected at a large number of discrete foci throughout the
nucleoplasm, extending to the nuclear envelope. During Sphase
and G2, the antigen is located in the nucleolus.
Double indirect immunofluorescence studies have revealed
that during early to mid G1 the Ki-67 antigen is associated
with reforming nucleoli within discrete domains which are
distinct from domains containing two of the major
nucleolar antigens fibrillarin and RNA polymerase I.
Within mature nucleoli the Ki-67 antigen is absent from
regions containing RNA polymerase I and displays only
partial co-localisation within domains containing either fibrillarin
or B23/nucleophosmin. Following disruption of
nucleolar structure, induced by treatment of cells with the
drug 5,6-dichloro-1-b-D-ribofuranosylbenzimidazole or
with actinomycin D, the Ki-67 antigen translocates to
nucleoplasmic foci which are associated with neither fibrillarin
nor RNA polymerase I. However, in treated cells
the Ki-67 Ag remains associated with, but not co-localised
to, regions containing B23/nucleophosmin. Our observations
suggest that the Ki-67 antigen associates with a fibrillarin-
deficient region of the dense fibrillar component of
the nucleolus. Integrity of this region is lost following either
nucleolar dispersal or nucleolar segregation
Quantifying the ki-67 heterogeneity profile in prostate cancer.
BackgroundKi-67 is a robust predictive/prognostic marker in prostate cancer; however, tumor heterogeneity in prostate biopsy samples is not well studied.MethodsUsing an MRI/US fusion device, biopsy cores were obtained systematically and by targeting when indicated by MRI. Prostate cores containing cancer from 77 consecutive men were analyzed. The highest Ki-67 was used to determine interprostatic variation. Ki-67 range (highest minus lowest) was used to determine intraprostatic and intralesion variation. Apparent diffusion coefficient (ADC) values were evaluated in relation to Ki-67.ResultsInterprostatic Ki-67 mean Ā± standard deviation (SD) values for NCCN low (L), intermediate (I), and high (H) risk patients were 5.1 Ā± 3.8%, 7.4 Ā± 6.8%, and 12.0 Ā± 12.4% (ANOVA P = 0.013). Intraprostatic mean Ā± SD Ki-67 ranges in L, I, and H risk patients were 2.6 Ā± 3.6%, 5.3 Ā± 6.8%, and 10.9 Ā± 12.3% (ANOVA P = 0.027). Intralesion mean Ā± SD Ki-67 ranges in L, I, and H risk patients were 1.1 Ā± 0.9%, 5.2 Ā± 7.9%, and 8.1 Ā± 10.8% (ANOVA P = 0.22). ADC values at Ki-67 > and <7.1% were 860 Ā± 203 and 1036 Ā± 217, respectively (P = 0.0029).ConclusionsHigh risk patients have significantly higher inter- and intraprostatic Ki-67 heterogeneity. This needs to be considered when utilizing Ki-67 clinically
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Expression of proliferation-dependent antigens during cellular ageing of normal and progeroid human fibroblasts
Normal human fibroblasts display a limited lifespan in
culture, which is due to a steadily decreasing fraction of
cells that are able to proliferate. Using antibodies that react
with antigens present in proliferating cells only, in an
indirect immunofluorescence assay, we have estimated the
fraction of proliferating cells in cultures of normal human
fibroblasts. Furthermore, we have estimated the rate of
decline in the fraction of proliferating cells during the
process of cellular ageing by application of the assay to
normal human fibroblasts throughout their lifespan in
culture. Wernerās Syndrome is an autosomal recessive
disease in which individuals display symptoms of ageing
prematurely. Wernerās Syndrome fibroblasts display a
reduced lifespan in culture compared with normal human
fibroblasts. Like normal human fibroblasts, the growth of
Wernerās Syndrome fibroblasts is characterised by a
decreasing fraction of cells reacting with the proliferationassociated
antibodies throughout their lifespan in culture.
However, the rate of loss of proliferating cells in Wernerās
Syndrome fibroblasts during the process of cellular ageing
is accelerated 5- to 6-fold compared with the rate determined
for normal human fibroblasts
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