1,126 research outputs found
DWH-DIM: A Blockchain Based Decentralized Integrity Verification Model for Data Warehouses
Data manipulation is often considered a serious
problem in industrial applications as data tampering can lead
to inaccurate financial reporting or even a corporate security
crisis. A correct representation of company data is essential
for the companies’ core business processes and is requested
by governments and investors. However, the current solution,
third-party auditing, is expensive and cannot be fully trusted.
In this paper, we present the Data Warehouse Decentralized
Integrity Model (DWH-DIM) to validate the integrity of the
data warehouse and replace the current process. To address
the challenge that the existing distributed integrity verification
models cannot handle GDPR and are limited by scalability,
our model uses a distributed file system to store attributes that
can be used for the integrity verification task. The blockchain
further confirms the authenticity of the files. Based on the
proposed model, we present a detailed implementation of the
DWH-DIM tool. The implementation is tested with a use case
and several benchmarks. Experimental results demonstrate that
our proposed model is feasible and meets the requirement for
certificate warehouse data
Functional Callan-Symanzik equation for QED
An exact evolution equation, the functional generalization of the
Callan-Symanzik method, is given for the effective action of QED where the
electron mass is used to turn the quantum fluctuations on gradually. The usual
renormalization group equations are recovered in the leading order but no
Landau pole appears.Comment: 9 pages, no figure
Critical factors for liposome-incorporated tumour-associated antigens to induce protective tumour immunity to SL2 lymphoma cells in mice
Physical
and
immunogenic
properties
of
re-
constituted
membranes
designed
for
the
presentation
of
tumour-associated
antigens
(TAA)
to
the
immune
system
are
described.
Proteins
and
lipids
of
crude
membranes
of
SL2
routine
lymphosarcoma
cells
were
partially
solubi-
lized
with
octylglucoside.
Reconstituted
membranes,
con-
sisting
mainly
of
unilamellar
vesicles
with
a
diameter
of
0.03-0.15
gm,
were
formed
by
detergent
removal
and
were
purified
by
floatation
in
a
discontinuous
sucrose
gra-
dient
to
remove
non-lipid-bound
protein.
Subcutaneous
immunization
of
syngeneic
mice
with
reconstituted
mem-
branes
or
with
purified
reconstituted
membranes
induced
protection
against
an
intraperitoneal
challenge
with
103
viable
SL2
cells.
Reconstituted
membranes
were
more
im-
munogenic
than
crude
membranes
in
immunoprotection
experiments
when
compared
on
the
basis
of
protein
dose.
Detergent
removal
was
required
to
obtain
an
immunogenic
presentation
form
of
SL2
membrane
antigens
and
to
avoid
toxicity
associated
with
the
detergent.
Reconstitution
of
SL2
membranes
in
the
presence
of
exogenous
phos-
pholipid
slightly
increased
the
fraction
of
protein
that
as-
sociated
with
the
reconstituted
membranes.
However,
the
immunogenicity
of
the
solubilized
membrane
TAA
was
not
significantly
affected
by
the
presence
of
exogenous
phospholipid.
The
reconstitution
procedure
described
may
be
useful
in
identifying
membrane
factors
required
for
the
induction
of
immune
responses
against
TAA.
The
versatil-
ity
of
the
system
may
be
employed
to
develop
safe
alterna-
tives
for
whole-cell
vaccines
Dose-dependent effects of Allopurinol on human foreskin fibroblast cell and human umbilical vein endothelial cell under hypoxia
Allopurinol, an inhibitor of xanthine oxidase, has been used in clinical trials of patients with cardiovascular and chronic kidney disease. These are two pathologies with extensive links to hypoxia and activation of the transcription factor hypoxia inducible factor (HIF) family. Here we analysed the effects of allopurinol treatment in two different cellular models, and their response to hypoxia. We explored the dose-dependent effect of allopurinol on Human Foreskin Fibroblasts (HFF) and Human Umbilical Vein Endothelial Cells (HUVEC) under hypoxia and normoxia. Under normoxia and hypoxia, high dose allopurinol reduced the accumulation of HIF-1α protein in HFF and HUVEC cells. Allopurinol had only marginal effects on HIF-1α mRNA level in both cellular systems. Interestingly, allopurinol effects over the HIF system were independent of prolyl-hydroxylase activity. Finally, allopurinol treatment reduced angiogenesis traits in HUVEC cells in an in vitro model. Taken together these results indicate that high doses of allopurinol inhibits the HIF system and pro-angiogenic traits in cells
Deciphering a subgroup of breast carcinomas with putative progression of grade during carcinogenesis revealed by comparative genomic hybridisation (CGH) and immunohistochemistry
Distinct parallel cytogenetic pathways in breast carcinogenesis could be identified in recent years. Nevertheless, it remained unclear as to which tumours may have progressed in grade or which patterns of cytogenetic alteration may define the switch from an in situ towards an invasive lesion. In order to gain more detailed insights into cytogenetic mechanisms of the pathogenesis of breast cancer, the chromosomal imbalances of 206 invasive breast cancer cases were characterised by means of comparative genomic hybridisation (CGH). CGH data were subjected to hierarchical cluster analysis and the results were further compared with immunohistochemical findings on tissue arrays from the same breast cancer cases. The combined analysis of immunohistochemical and cytogenetic data provided evidence that carcinomas with gains of 7p, and to a lesser extent losses of 9q and gains of 5p, are a distinct subgroup within the spectrum of ductal invasive grade 3 breast carcinomas. These aberrations were associated with a high degree of cytogenetic instability (16.6 alterations per case on average), 16q-losses in over 70% of these cases, strong oestrogen receptor expression and absence of strong expression of p53, c-erbB2 and Ck 5. These characteristics provide strong support for the hypothesis that these tumours may develop through stages of well- and perhaps intermediately differentiated breast cancers. Our results therefore underline the existence of several parallel and also stepwise progression pathways towards breast cancer
P-rex1 cooperates with PDGFRβ to drive cellular migration in 3D microenvironments
Expression of the Rac-guanine nucleotide exchange factor (RacGEF), P-Rex1 is a key determinant of progression to metastasis in a number of human cancers. In accordance with this proposed role in cancer cell invasion and metastasis, we find that ectopic expression of P-Rex1 in an immortalised human fibroblast cell line is sufficient to drive multiple migratory and invasive phenotypes. The invasive phenotype is greatly enhanced by the presence of a gradient of serum or platelet-derived growth factor, and is dependent upon the expression of functional PDGF receptor β. Consistently, the invasiveness of WM852 melanoma cells, which endogenously express P-Rex1 and PDGFRβ, is opposed by siRNA of either of these proteins. Furthermore, the current model of P-Rex1 activation is advanced through demonstration of P-Rex1 and PDGFRβ as components of the same macromolecular complex. These data suggest that P-Rex1 has an influence on physiological migratory processes, such as invasion of cancer cells, both through effects upon classical Rac1-driven motility and a novel association with RTK signalling complexes
Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression
Endothelial Wnt/β-catenin signaling is necessary for angiogenesis of the central nervous system and blood–brain barrier (BBB) differentiation, but its relevance for glioma vascularization is unknown. In this study, we show that doxycycline-dependent Wnt1 expression in subcutaneous and intracranial mouse glioma models induced endothelial Wnt/β-catenin signaling and led to diminished tumor growth, reduced vascular density, and normalized vessels with increased mural cell attachment. These findings were corroborated in GL261 glioma cells intracranially transplanted in mice expressing dominant-active β-catenin specifically in the endothelium. Enforced endothelial β-catenin signaling restored BBB characteristics, whereas inhibition by Dkk1 (Dickkopf-1) had opposing effects. By overactivating the Wnt pathway, we induced the Wnt/β-catenin–Dll4/Notch signaling cascade in tumor endothelia, blocking an angiogenic and favoring a quiescent vascular phenotype, indicated by induction of stalk cell genes. We show that β-catenin transcriptional activity directly regulated endothelial expression of platelet-derived growth factor B (PDGF-B), leading to mural cell recruitment thereby contributing to vascular quiescence and barrier function. We propose that reinforced Wnt/β-catenin signaling leads to inhibition of angiogenesis with normalized and less permeable vessels, which might prove to be a valuable therapeutic target for antiangiogenic and edema glioma therapy
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