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"Wang, Chen-yu"
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Lee Kuan Yew through the eyes of Chinese scholars
\"A compilation of essays by highly-respected Chinese scholars in which they evaluate the life, work and philosophy of Lee Kuan Yew, founding Prime Minister of Singapore. Presenting a range of views from a uniquely Chinese/Asian perspective, this book provides valuable insights for those who wish to gain a fuller and deeper understanding of Lee Kuan Yew, the man, as well as Singapore, his nation\"-- Provided by publisher.
Book
Targeting monoamine oxidase A-regulated tumor-associated macrophage polarization for cancer immunotherapy
Targeting tumor-associated macrophages (TAMs) is a promising strategy to modify the immunosuppressive tumor microenvironment and improve cancer immunotherapy. Monoamine oxidase A (MAO-A) is an enzyme best known for its function in the brain; small molecule MAO inhibitors (MAOIs) are clinically used for treating neurological disorders. Here we observe MAO-A induction in mouse and human TAMs. MAO-A-deficient mice exhibit decreased TAM immunosuppressive functions corresponding with enhanced antitumor immunity. MAOI treatment induces TAM reprogramming and suppresses tumor growth in preclinical mouse syngeneic and human xenograft tumor models. Combining MAOI and anti-PD-1 treatments results in synergistic tumor suppression. Clinical data correlation studies associate high intratumoral
MAOA
expression with poor patient survival in a broad range of cancers. We further demonstrate that MAO-A promotes TAM immunosuppressive polarization via upregulating oxidative stress. Together, these data identify MAO-A as a critical regulator of TAMs and support repurposing MAOIs for TAM reprogramming to improve cancer immunotherapy.
Monoamine oxidase A (MAO-A) is an outer mitochondrial membrane-bound enzyme best known for its function in the brain, but also linked to cancer progression. Here, the authors show that MAO-A is expressed in tumor associated macrophages, promoting their immunosuppressive properties, and that MAO inhibition suppresses tumor growth in preclinical models.
Journal Article
Effects of phosphorus-modified biochar as a soil amendment on the growth and quality of Pseudostellaria heterophylla
Phosphorus (P) deficiency in agricultural soil is a worldwide concern. P modification of biochar, a common soil conditioner produced by pyrolysis of wastes and residues, can increase P availability and improve soil quality. This study aims to investigate the effects of P-modified biochar as a soil amendment on the growth and quality of a medicinal plant (
Pseudostellaria heterophylla
).
P. heterophylla
were grown for 4 months in lateritic soil amended with P-modified and unmodified biochar (peanut shell) at dosages of 0, 3% and 5% (by mass). Compared with unmodified biochar, P-modified biochar reduced available heavy metal Cd in soil by up to 73.0% and osmotic suction in the root zone by up to 49.3%. P-modified biochar application at 3% and 5% promoted the tuber yield of
P. heterophylla
significantly by 68.6% and 136.0% respectively. This was different from that in unmodified biochar treatment, where tuber yield was stimulated at 3% dosage but inhibited at 5% dosage. The concentrations of active ingredients (i.e., polysaccharides, saponins) in tuber were increased by 2.9–78.8% under P-modified biochar amendment compared with control, indicating the better tuber quality. This study recommended the application of 5% P-modified biochar for promoting the yield and quality of
P. heterophylla
.
Journal Article
Reciprocity, evolution, and decision games in network and data science
\"Learn how to analyze and manage evolutionary and sequential user behaviors in modern networks, and how to optimize network performance by using indirect reciprocity, evolutionary games, and sequential decision-making. Understand the latest theory without the need to go through the details of traditional game theory. With practical management tools to regulate user behavior and simulations and experiments with real data sets, this is an ideal tool for graduate students and researchers working in networking, communications, and signal processing\"-- Provided by publisher.
Book
PRC1 collaborates with SMCHD1 to fold the X-chromosome and spread Xist RNA between chromosome compartments
X-chromosome inactivation triggers fusion of A/B compartments to inactive X (Xi)-specific structures known as S1 and S2 compartments. SMCHD1 then merges S1/S2s to form the Xi super-structure. Here, we ask how S1/S2 compartments form and reveal that Xist RNA drives their formation via recruitment of Polycomb repressive complex 1 (PRC1). Ablating
Smchd1
in post-XCI cells unveils S1/S2 structures. Loss of SMCHD1 leads to trapping Xist in the S1 compartment, impairing RNA spreading into S2. On the other hand, depleting Xist, PRC1, or HNRNPK precludes re-emergence of S1/S2 structures, and loss of S1/S2 compartments paradoxically strengthens the partition between Xi megadomains. Finally, Xi-reactivation in post-XCI cells can be enhanced by depleting both SMCHD1 and DNA methylation. We conclude that Xist, PRC1, and SMCHD1 collaborate in an obligatory, sequential manner to partition, fuse, and direct self-association of Xi compartments required for proper spreading of Xist RNA.
The inactive X (Xi)-specific S1/S2 chromosome compartments are merged by SMCHD1, but how the S1/S2 structure is constructed is unclear. The authors find that PRC1 drives the formation of S1/S2s and that the stepwise folding process of the Xi facilitates Xist RNA spreading between Xi compartments.
Journal Article
NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review
The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonical but also non-canonical NF-κB pathways. To initiate both of these pathways, IκB-degradation triggers NF-κB release and the nuclear translocated-heterodimer (or homodimer) can associate with the κB sites of promoter to regulate the gene transcriptions. NF-κB ubiquitously expresses in neurons and the constitutive NF-κB activation is associated with processing of neuronal information. NF-κB can regulate the transcription of genes such as chemokines, cytokines, proinflammatory enzymes, adhesion molecules, proinflammatory transcription factors, and other factors to modulate the neuronal survival. In neuronal insult, NF-κB constitutively active in neuron cell bodies can protect neurons against different injuries and regulate the neuronal inflammatory reactions. Besides neurons, NF-κB transcription factors are abundant in glial cells and cerebral blood vessels and the diverse functions of NF-κB also regulate the inflammatory reaction around the neuronal environment. NF-κB transcription factors are abundant in the brain and exhibit diverse functions. Several central nerve system (CNS) diseases are linked to NF-κB activated by inflammatory mediators. The RelA and c-Rel expression produce opposite effects on neuronal survival. Importantly, c-Rel expression in CNS plays a critical role in anti-apoptosis and reduces the age-related behaviors. Moreover, the different subunits of NF-κB dimer formation can modulate the neuroninflammation, neuronal protection, or neurotoxicity. The diverse functions of NF-κB depend on the subunits of the NF-κB dimer-formation which enable us to develop a therapeutic approach to neuroinflammation based on a new concept of inflammation as a strategic tool in neuronal cells. However, the detail role of NF-κB in neuroinflammation, remains to be clarified. In the present article, we provide an updated review of the current state of our knowledge about relationship between NF-κB and neuroinflammation.
Journal Article
Top quark contribution to two-loop helicity amplitudes for Z boson pair production in gluon fusion
A
bstract
We compute the top quark contribution to the two-loop amplitude for on-shell
Z
boson pair production in gluon fusion,
gg → ZZ
. Exact dependence on the top quark mass is retained. For each phase space point the integral reduction is performed numerically and the master integrals are evaluated using the auxiliary mass flow method, allowing fast computation of the amplitude with very high precision.
Journal Article
Kernel Selection for Gaussian Process in Cosmology: With Approximate Bayesian Computation Rejection and Nested Sampling
The Gaussian process (GP) has gained much attention in cosmology due to its ability to reconstruct cosmological data in a model-independent manner. In this study, we compare two methods for GP kernel selection: approximate Bayesian computation (ABC) rejection and nested sampling. We analyze three types of data: cosmic chronometer data, type Ia supernovae data, and gamma-ray burst data, using five kernel functions. To evaluate the differences between kernel functions, we assess the strength of evidence using Bayes factors. Our results show that, for ABC rejection, the Matérn kernel with ν = 5/2 (M52 kernel) outperformes the commonly used radial basis function (RBF) kernel in approximating all three data sets. Bayes factors indicate that the M52 kernel typically supports the observed data better than the RBF kernel but with no clear advantage over other alternatives. However, nested sampling gives different results, with the M52 kernel losing its advantage. Nevertheless, Bayes factors indicate no significant dependence of the data on each kernel.
Journal Article
Contribution of third generation quarks to two-loop helicity amplitudes for W boson pair production in gluon fusion
A
bstract
We compute the contribution of third generation quarks (
t, b
) to the two-loop amplitude for on-shell
W
boson pair production in gluon fusion
gg → WW
. We present plots for the amplitude across partonic phase space as well as reference values for two kinematic points. The master integrals are efficiently evaluated by numerically solving a system of ordinary differential equations.
Journal Article