243 research outputs found
The desmosome and pemphigus
Desmosomes are patch-like intercellular adhering junctions (“maculae adherentes”), which, in concert with the related adherens junctions, provide the mechanical strength to intercellular adhesion. Therefore, it is not surprising that desmosomes are abundant in tissues subjected to significant mechanical stress such as stratified epithelia and myocardium. Desmosomal adhesion is based on the Ca2+-dependent, homo- and heterophilic transinteraction of cadherin-type adhesion molecules. Desmosomal cadherins are anchored to the intermediate filament cytoskeleton by adaptor proteins of the armadillo and plakin families. Desmosomes are dynamic structures subjected to regulation and are therefore targets of signalling pathways, which control their molecular composition and adhesive properties. Moreover, evidence is emerging that desmosomal components themselves take part in outside-in signalling under physiologic and pathologic conditions. Disturbed desmosomal adhesion contributes to the pathogenesis of a number of diseases such as pemphigus, which is caused by autoantibodies against desmosomal cadherins. Beside pemphigus, desmosome-associated diseases are caused by other mechanisms such as genetic defects or bacterial toxins. Because most of these diseases affect the skin, desmosomes are interesting not only for cell biologists who are inspired by their complex structure and molecular composition, but also for clinical physicians who are confronted with patients suffering from severe blistering skin diseases such as pemphigus. To develop disease-specific therapeutic approaches, more insights into the molecular composition and regulation of desmosomes are required
PCNA levels in neuroblastoma are increased in tumors with an amplified N- myc gene and in metastatic stage tumors
N- myc oncogene amplification in neuroblastoma has been found to be significantly associated with advanced stage disease and tumor progression. However, there is a lack of data on tumors, regarding the relationship between N- myc gene amplification and proliferation activity. Proliferating cell nuclear antigen (PCNA) is a proliferation-induced 36 kD nuclear protein that is the auxiliary component of DNA polymerase δ. PCNA levels in tissues have been found to correlate with proliferative activity. We have examined PCNA levels in neuroblastomas in relation to N- myc gene amplification and tumor stage. Statistically, significantly higher levels of PCNA were observed in tumors with an amplified N- myc gene relative to tumors with a single gene copy. The highest levels of PCNA were observed in advanced stage tumors with an amplified N- myc gene. Treatment of neuroblastoma cells in culture with retinoic acid, which induces differentiation, resulted in a substantial decrease in PCNA. Our results suggest that PCNA levels may reflect differences in proliferative activity between neuroblastomas, related to stage of the disease and to N- myc gene copy number.[/p ]Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42581/1/10585_2004_Article_BF00880069.pd
Changes of bed grain size distribution below hydraulic structure
The paper
presents results of laboratory investigations
of local scour in non-uniform non-cohesive
bed material below a horizontal solid apron. An experiment of local scouring conducted
in a glass-sided rectangular fl ume under clear-
water conditions with constant water discharge
was performed. In this study several
non-uniform soils consisted of the following
coloured fractions: 0.5–1.25, 1.25–2.5, 2.5–
–4.0, 4.0–6.3, and 6.3–10.0 mm were used.
Every scour hole had begun just below the
solid apron having mild slope and downward
concave shape. Similar changes in grain
composition were observed in all tests; the
hole bottom at the deepest section was covered
by the largest grains. During the experiments
it was found that bed armour coat
had formed in soils with standard deviation
of mean grain size σg > 2 and downstream of
the maximum scour hole depth, only. Soils
with σg < 2 did not create any armour coat,
and single coarse grains increased turbulence
behind them and accelerated erosion of fi ner
grains
Two separate genes regulate self-Ia and carrier recognition in H-2-restricted helper factors secreted by hybridoma cells
H-2 heterologous T cell hybridomas were used to study the genetic control of dual, anti-nominal antigen and anti-self H-2 specificity of H-2 restricted T cell factors. Each of four hybridoma clones produced two helper factors. One was restricted for the Ia type of the normal T cell partner (H-2b), whereas the other was restricted for the ia type of the lymphoma partner (H-2k) of the somatic hybrid. This was shown by affinity separation on parental type spleen cells and on monoclonal anti-I-A-Sepharose. Both factors had carrier (chicken gamma globulin; CGG)-specific helper effect, and both bound to anti-VH-315-Sepharose. Because the lymphoma (BW-5147) partner could not contribute a CGG- specific locus, the H-2k-restricted, CGG-specific factor had to be the product of segregating anti-nominal and anti-self loci. This suggests that dual specificity is due to two independent loci and support the validity of dual recognition concepts. Anti-self specificity was associated with homologous Ia alloantigens in the individual factors. Therefore, Ia and anti-self might be linked. Implications of the major histocompatibility complex or VH nature of anti-self receptors and the relationship of T cell factors and receptors was discussed
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