3,808 research outputs found
BuffGraph: Enhancing Class-Imbalanced Node Classification via Buffer Nodes
Class imbalance in graph-structured data, where minor classes are
significantly underrepresented, poses a critical challenge for Graph Neural
Networks (GNNs). To address this challenge, existing studies generally generate
new minority nodes and edges connecting new nodes to the original graph to make
classes balanced. However, they do not solve the problem that majority classes
still propagate information to minority nodes by edges in the original graph
which introduces bias towards majority classes. To address this, we introduce
BuffGraph, which inserts buffer nodes into the graph, modulating the impact of
majority classes to improve minor class representation. Our extensive
experiments across diverse real-world datasets empirically demonstrate that
BuffGraph outperforms existing baseline methods in class-imbalanced node
classification in both natural settings and imbalanced settings. Code is
available at https://anonymous.4open.science/r/BuffGraph-730A
The Viral Envelope Gene Is Involved in Macrophage Tropism of a Human Immunodeficiency Virus Type 1 Strain Isolated from Brain Tissue
Human immunodeficiency virus type 1 (HIV-1) strains isolated from the central nervous system (CNS) may represent a subgroup that displays a host cell tropism different from those isolated from peripheral blood and lymph nodes. One CNS-derived isolate, HIV-lSF128A , which can be propagated efficiently in primary macrophage culture but not in any T-cell lines, was molecularly cloned and characterized. Recombinant viruses between HIV-1SF128A and the peripheral blood isolate HIV-ISF2 were generated in order to map the viral gene(s) responsible for the macrophage tropism. The env gene sequences of the two isolates are about 91.1% homologous, with variations scattered mainly in the hypervariable regions of gp120. Recombinant viruses that have acquired the HIV-lSF128A env gene display HIV-1SF128A tropism for macrophages. Furthermore, the gp120 variable domains, V1, V2, V4, and V5, the CD4-binding domain, and the gp41 fusion domain are not directly involved in determining macrophage tropism
Integrating multi-type aberrations from DNA and RNA through dynamic mapping gene space for subtype-specific breast cancer driver discovery
Driver event discovery is a crucial demand for breast cancer diagnosis and
therapy. Especially, discovering subtype-specificity of drivers can prompt the
personalized biomarker discovery and precision treatment of cancer patients.
still, most of the existing computational driver discovery studies mainly
exploit the information from DNA aberrations and gene interactions. Notably,
cancer driver events would occur due to not only DNA aberrations but also RNA
alternations, but integrating multi-type aberrations from both DNA and RNA is
still a challenging task for breast cancer drivers. On the one hand, the data
formats of different aberration types also differ from each other, known as
data format incompatibility. One the other hand, different types of aberrations
demonstrate distinct patterns across samples, known as aberration type
heterogeneity. To promote the integrated analysis of subtype-specific breast
cancer drivers, we design a "splicing-and-fusing" framework to address the
issues of data format incompatibility and aberration type heterogeneity
respectively. To overcome the data format incompatibility, the "splicing-step"
employs a knowledge graph structure to connect multi-type aberrations from the
DNA and RNA data into a unified formation. To tackle the aberration type
heterogeneity, the "fusing-step" adopts a dynamic mapping gene space
integration approach to represent the multi-type information by vectorized
profiles. The experiments also demonstrate the advantages of our approach in
both the integration of multi-type aberrations from DNA and RNA and the
discovery of subtype-specific breast cancer drivers. In summary, our
"splicing-and-fusing" framework with knowledge graph connection and dynamic
mapping gene space fusion of multi-type aberrations data from DNA and RNA can
successfully discover potential breast cancer drivers with subtype-specificity
indication.Comment: 14 pages, 5 figures, 1 tabl
Vertical Structure of Neutrino Dominated Accretion Disks and Neutrino Transport in the disks
We investigate the vertical structure of neutrino dominated accretion disks
by self-consistently considering the detailed microphysics, such as the
neutrino transport, vertical hydrostatic equilibrium, the conservation of
lepton number, as well as the balance between neutrino cooling, advection
cooling and viscosity heating. After obtaining the emitting spectra of
neutrinos and antineutrinos by solving the one dimensional Boltzmann equation
of neutrino and antineutrino transport in the disk, we calculate the
neutrino/antineutrino luminosity and their annihilation luminosity. We find
that the total neutrino and antineutrino luminosity is about ergs/s
and their annihilation luminosity is about ergs/s with an
extreme accretion rate /s and an alpha viscosity
. In addition, we find that the annihilation luminosity is
sensitive to the accretion rate and will not exceed ergs/s which is
not sufficient to power the most fireball of GRBs, if the accretion rate is
lower than /s. Therefore, the effects of the spin of black
hole or/and the magnetic field in the accretion flow might be introduced to
power the central engine of GRBs.Comment: 22 pages, 9 figures, ApJ accepte
4,4′-MethylÂenedianilinium bisÂ(3-carbÂoxy-4-hydroxyÂbenzeneÂsulfonate) monohydrate
Co-crystallization of 4,4′-methylÂenediphenylÂamine (MDA) and 5-sulfosalicylic acid (5-H2SSA) yields the title salt, C13H16N2
2+·2C7H5O6S−·H2O. The asymmetric unit is comprised of one dication, two anions and one water molÂecule. In the crystal structure, the components of the salt are linked by a combination of interÂmolecular O—H⋯O, N—H⋯O and weak C—H⋯O hydrogen bonds into a three-dimensional framework. In addition, two weak π–π interÂactions [with centroid–centroid distances of 3.8734 (15) and 3.7465 (15) Å] and one C—H⋯π interÂaction further stabilize the crystal structure
The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK
Introduction. This study endeavors to analyze the effects of miR-1204 on the expression of DEK oncogene in non-small cell lung cancer (NSCLC) cell lines and to study the molecular mechanisms of these effects.
Material and methods. The miR-1204 mimics and inhibitors were transfected into the (A549 and SPC) NSCLC cells. Then the mRNA levels, cell viability, apoptosis rate, morphology and caspase activity were determined. The expression of apoptosis-related proteins Bcl-2 and Bax was also analyzed.
Results. In NSCLC cell lines (A549 and SPC), DEK mRNA levels were down-regulated in miR-1204 overexÂpression group. In miR-1204 inhibition group, the expression of DEK mRNA showed an opposite trend. The overexpression of miR-1204 increases the apoptosis rate in NSCLC cells. The Bcl-2 levels in the miR-1204 overÂexpression group were decreased, while the Bax level was increased. In the miR-1204 inhibition group, expression of Bcl-2 and Bax showed opposite trends. Cell staining revealed cell’s morphological changes; the apoptosis in the miR-1204 overexpression group revealed significant morphological features, such as brighter nuclei and nuÂclear condensation. Results indicated a typical characteristic of apoptosis in the miR-1204 overexpression group. Caspase-9 and Caspase-3 were involved in the apoptosis pathway, which was mediated by miR-1204 and DEK.
Conclusions. The miR-1204 induces apoptosis of NSCLC cells by inhibiting the expression of DEK. The mechÂanism of apoptosis involves down-regulation of Bcl-2 and up-regulation of Bax expression. Moreover, the apoptosis was mediated by mitochondria-related caspase 9/3 pathway
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