Inert Higgs Dark Matter for CDF II W-Boson Mass and Detection Prospects.

The W-boson mass, which was recently measured at Fermilab with an unprecedented precision, suggests the presence of new multiplets beyond the standard model (SM). One of the minimal extensions of the SM is to introduce an additional scalar doublet in which the non-SM scalars can enhance W-boson mass via the loop corrections. On the other hand, with a proper discrete symmetry, the lightest new scalar in the doublet can be stable and play the role of a dark matter particle. We show that the inert two Higgs doublet model can naturally handle the new W-boson mass without violating other constraints and that the preferred dark matter mass is between 54 and 74 GeV. We identify three feasible parameter regions for the thermal relic density: the SA coannihilation, the Higgs resonance, and the SS→WW^{*} annihilation. We find that the first region can be fully tested by the High Luminosity Large Hadron Collider, the second region will be tightly constrained by direct detection experiments, and the third region could yield detectable GeV γ-ray and antiproton signals in the Galaxy that may have been observed by the Fermi Large Area Telescope and the Alpha Magnetic Spectrometer AMS-02 experiment.

Possible Dark Matter Annihilation Signal in the AMS-02 Antiproton Data.

Using the latest AMS-02 cosmic-ray antiproton flux data, we search for a potential dark matter annihilation signal. The background parameters about the propagation, source injection, and solar modulation are not assumed a priori but based on the results inferred from the recent B/C ratio and proton data measurements instead. The possible dark matter signal is incorporated into the model self-consistently under a Bayesian framework. Compared with the astrophysical background-only hypothesis, we find that a dark matter signal is favored. The rest mass of the dark matter particles is ∼20-80 GeV, and the velocity-averaged hadronic annihilation cross section is about (0.2-5)×10^{-26} cm^{3} s^{-1}, in agreement with that needed to account for the Galactic center GeV excess and/or the weak GeV emission from dwarf spheroidal galaxies Reticulum 2 and Tucana III. Tight constraints on the dark matter annihilation models are also set in a wide mass region.

Mirror QCD phase transition as the origin of the nanohertz Stochastic Gravitational-Wave Background.

Several Pulsar Timing Array (PTA) Collaborations have recently provided strong evidence for a nHz Stochastic Gravitational-Wave Background (SGWB). Here we investigate the implications of a first-order phase transition occurring within the early Universe's dark quantum chromodynamics epoch, specifically within the framework of the mirror twin Higgs dark sector model. Our analysis indicates a distinguishable SGWB signal originating from this phase transition, which can explain the measurements obtained by PTAs. Remarkably, a significant portion of the parameter space for the SGWB signal also effectively resolves the existing tensions in both the H0 and S8 measurements in Cosmology. This intriguing correlation suggests a possible common origin of these three phenomena for 0.2<ΔNeff<0.5, where the mirror dark matter component constitutes less than 30% of the total dark matter abundance. Next-generation CMB experiments such as CMB-S4 can test this parameter region.

A common origin of muon g-2 anomaly, Galaxy Center GeV excess and AMS-02 anti-proton excess in the NMSSM.

The supersymmetric model is one of the most attractive extensions of the Standard Model of particle physics. In light of the most recently reported anomaly of the muon g-2 measurement by the FermiLab E989 experiment, and the excesses of gamma rays at the Galactic center observed by Fermi-LAT space telescope, as well as the antiproton excess observed by the Alpha Magnetic Spectrometer, we propose to account for all these anomalies or excesses in the Next-to-Minimal Supersymmetric Standard Model (NMSSM). Considering various experimental constraints including the Higgs mass, B-physics, collider data, dark matter relic density and direct detections, we find that a ~60 GeV bino-like neutralino is able to successfully explain all these observations. Our scenario can be sensitively probed by future direct detection experiments.

Decreased expression of UK114 is related to the differentiation status of human hepatocellular carcinoma.

Previous studies have identified that the expression of UK114 is tissue specific and the protein has been found to be most abundant in liver and kidney. However, the expression of UK114 in human hepatocellular carcinoma and its relationship to differentiation and transformation of hepatocellular carcinoma have not been studied. In this study, the expression of UK114 in human hepatocellular carcinoma was examined by Northern and Western blot analyses. We found that UK114 was significantly down-regulated in most of hepatocellular carcinoma tissues compared with adjacent nontumor tissues (72.7%) at both mRNA and protein levels. We looked into the possibility that this decreased expression of UK114 in the hepatocellular carcinoma tissues may play a role in the differentiation or tumorigenicity of hepatocellular carcinoma. Immunohistochemical staining showed that the reduced expression of UK114 in hepatocellular carcinoma tissues was correlated with the tumor differentiation status as graded by the Edmondson-Steiner classification. On the other hand, overexpression of UK114 was not able to suppress the proliferation of human hepatoma cells and tumorigenicity in nude mice. These results suggest that UK114 does not seem to act as a tumor suppressor gene; however, it may useful as a biomarker that will assist in the grading of the differentiation status of hepatocellular carcinoma samples.

One single nucleotide difference alters the differential expression of spliced RNAs between HBV genotypes A and D.

Hepatitis B virus (HBV) is generally classified into eight genotypes (A to H) based on genomic sequence divergence. The sequence variation among the different HBV genotypes suggests that the spliced RNAs should be different from genotype to genotype. However, the cis-acting element involved in the modulation of the distinct expression profiles of spliced HBV RNAs remains unidentified. Moreover, the biological role of splicing in the life cycle of HBV is not yet understood. In this study, spliced RNAs generated from genotypes A and D were carefully characterized in transfected HepG2 cells. The species and frequency of the spliced RNAs were dramatically different in the two genotypes. Of note, a population of multiply spliced RNAs with intron 2067-2350 excision was identified in HBV genotype A-transfected HepG2 cells, but not in genotype D transfected HepG2 cells. Further, we found a single nucleotide difference (2335) located within the polypyrimidine tract of the splice acceptor site 2350 between the two genotypes, and a single base substitution at 2335 was able to convert the splicing pattern of genotype D (or genotype A) to that of genotype A (or genotype D). These findings suggest that different unique splice sites may be preferentially used in different HBV genotypes resulting in distinct populations of spliced RNAs. The possible significance of the distinct spliced RNAs generated from the different HBV genotypes in HBV infection is discussed.

HNF-4α determines hepatic differentiation of human mesenchymal stem cells from bone marrow.

AIM: To investigate the differentiation status and key factors to facilitate hepatic differentiation of human bone-marrow-derived mesenchymal stem cells (MSCs). METHODS: Human MSCs derived from bone marrow were induced into hepatocyte-like cells following a previously published protocol. The differentiation status of the hepatocyte-like cells was compared with various human hepatoma cell lines. Overexpression of hepatocyte nuclear factor (HNF)-4α was mediated by adenovirus infection of these hepatocyte-like cells. The expression of interesting genes was then examined by either reverse transcription-polymerase chain reaction (RT-PCR) or real-time RT-PCR methods. RESULTS: Our results demonstrated that the differentiation status of hepatocyte-like cells induced from human MSCs was relatively similar to poorly differentiated human hepatoma cell lines. Interestingly, the HNF-4 isoform in induced MSCs and poorly differentiated human hepatoma cell lines was identified as HNF-4γ instead of HNF-4α. Overexpression of HNF-4α in induced MSCs significantly enhanced the expression level of hepatic-specific genes, liver-enriched transcription factors, and cytochrome P450 (P450) genes. CONCLUSION: Overexpression of HNF-4α improves the hepatic differentiation of human MSCs from bone marrow and is a simple way of providing better cell sources for clinical applications.

Transforming growth factor-beta1 suppresses hepatitis B virus replication primarily through transcriptional inhibition of pregenomic RNA.

UNLABELLED: Transforming growth factor-beta1 (TGF-beta1) is a pleiotropic cytokine with pivotal roles in the regulation of cellular functions and immune responses. In this study, we found that TGF-beta1 was able to effectively suppress hepatitis B virus (HBV) replication. In the presence of TGF-beta1, the level of viral replicative intermediates was dramatically decreased, both in actively dividing cells and in confluent cells. At the same time, the levels of viral transcripts, core protein, and nucleocapsid were significantly diminished by TGF-beta1 treatment. Interestingly, the inhibitory activity of TGF-beta1 was associated with preferential reduction of the level of pregenomic RNA compared with pre-C mRNA. Further analysis indicated that TGF-beta1 might exert its antiviral effect primarily through reducing expression of the HBV core protein by transcriptional regulation instead of posttranscriptional modification. CONCLUSION: TGF-beta1 may play a dual role in HBV infection, in the suppression of immune responses against viral infection and in the direct inhibition of viral replication, resulting in minimization of liver damage in patients with chronic hepatitis.