1,721,057 research outputs found
Effects of gliadin stimulation on bone marrow-derived dendritic cells from HLA-DQ8 transgenic MICE
Gliadin presentation by HLA-DQ2/8 molecules to T cells plays a crucial role in triggering the inflammatory cascade in coeliac disease. We aimed to study the immunological effects of gliadin stimulation on dendritic cells (DCs) from HLA-DQ8 transgenic and BALB/c mice
“Analisi funzionale e fenotipica di splenociti e leucociti mononucleati di sangue periferico di pollo”.
Identification of an optimal concentration of platelet gel for promoting angiogenesis in human endothelial cells
In recent years, numerous studies have supported
the use of topical blood components to improve
wound healing and tissue regeneration. Platelet gel
(PG), a hemocomponent obtained from mix of
activated platelets (PLTs) and cryoprecipitate,1 is currently
being used clinically in reconstructive, cosmetic, orthopedic,
cardiovascular, oral maxillofacial, and dermatologic
surgery in an attempt to improve tissue healing.2,3 PLTs
have concentrated levels of naturally occurring growth
factors and other substances that have the potential to
accelerate tissue repair4-6 by influencing several cellular
processes including chemotaxis, cell proliferation, cell differentiation,
angiogenesis, matrix deposition, and tissue
remodeling.7,8
Previous studies have demonstrated that the healing
process might be accelerated by the use of PG. Compared
with lesions of patients treated by conventional methods,
the sternal dehiscent wounds and skin necrotic ulcers of patients treated with PG recovered more rapidly.9 Moreover,
patients treated by partial mandibulectomies for
malignant tumors experienced satisfactory mandibular
reconstructions when PLT-rich plasma was combined
with autologous bone grafts.10
Despite the promising clinical results, PG use has
proceeded in a totally empirical way, mainly grounding
on experience of individual doctors, and the most effective
PG concentration to promote wound healing has
not yet been determined. In this study, the effects of
PG-released supernatant at different concentrations on
angiogenesis (process involved in tissue reparation
mechanism) were investigated using different in vitro
assays (proliferation, migration, invasion, cord formation,
and wound healing)
suPAR, a soluble form of urokinase plasminogen activator receptor, inhibits human prostate cancer cell growth and invasion
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Induction of a multifactorial resistance phenotype by high paclitaxel selective pressure in a human ovarian carcinoma cell line
Cathepsin B mediates the pH-dependent proinvasive activity of tumor-shed microvesicles
Vesicles shed by cancer cells are known to mediate several tumor-host interactions. Tumor microenvironment
may, in turn, influence the release and the activity of tumor-shed microvesicles. In this study, we investigated
the molecular mediators of the pH-dependent proinvasive activity of tumor-shed vesicles. Gelatinase zymography
showed increased microvesicle activity of matrix metalloproteinases 9 and 2 as a result of acid exposure (pH 5.6)
compared to pH 7.4. Thus, we reasoned that the cysteine protease cathepsin B might play a role in mediating the
pH-dependent activation of gelatinases. Cathepsin B expression in tumor-shed microvesicles was confirmed by
Western blot analysis and zymography. The activity of vesicle-associated cathepsin B measured using Z-Arg-
Arg-pNA as substrate was significantly increased at acidic pH values. Inhibition of protease activity by the cysteine
protease inhibitor, E-64, and treatment of ovarian cancer cells with small interfering RNA against cathepsin B suppressed
the ability of tumor-shed microvesicles to stimulate both gelatinase activation and the invasiveness of
endothelial cells observed at low pH values. We conclude that microvesicle shedding is a major secretory pathway
for cathepsin B release from tumor cells. Hence, the acidic microenvironment found in most solid tumors may
contribute to cathepsin B–mediated proinvasive capabilities of tumor-shed vesicle
Akt down-modulation induces apoptosis of human prostate cancer cells and synergizes with EGFR tyrosine kinase inhibitors
BACKGROUND. PTEN is a well-characterized tumor suppressor that negatively regulates cell growth and survival through the modulation of PI3K/Akt pathway. METHODS. In this paper, we investigated the effects of an PI3K/Akt inhibitor, perifosine, in human prostate cancer (PCa) cells analyzing cell proliferation, apoptosis, and the synergy with EGFR inhibitors. RESULTS. Clinically achievable concentrations of perifosine, as well as Akt gene knockdown, induced a G0/G1 arrest and apoptosis in PTEN defective PCa cells. Although PTEN introduction was able to restore the control of Akt activity and to reduce cell proliferation, the manipulation of PTEN gene was not able alone to influence apoptosis. Perifosine induced apoptotic program also in PTEN positive cells when Akt activity was augmented by EGF suggesting the possibility that this drug could be used in combination with EGFR inhibitors. The combination treatment between erlotinib and pharmacological or molecular Akt knockdown, indeed, showed synergistic effects. This is the first demonstration that a pharmacological compound against Akt activity can restore the efficacy against EGFR inhibitors in PCa and has important therapeutic fallout since EGFR inhibitors have demonstrated very low effectiveness in PCa patients. CONCLUSIONS. Taken together our data have an important clinical relevance in the treatment of advanced prostate tumors. However, further studies in the setting of combination therapies in advanced PCas are necessary
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