Probing dark particles indirectly at the CEPC

When dark matter candidate and its parent particles are nearly degenerate, it would be difficult to probe them at the Large Hadron Collider directly. We propose to explore their quantum loop effects at the CEPC through the golden channel process $e^+e^-\to \mu^+\mu^-$. We use a renormalizable toy model consisting of a new scalar and a fermion to describe new physics beyond the Standard Model. The new scalar and fermion are general multiplets of the $SU(2)_L\times U(1)_Y$ symmetry, and couple to the muon lepton through Yukawa interaction. We calculate their loop contributions to anomalous $\gamma\mu^+\mu^-$ and $Z\mu^+\mu^-$ couplings which can be applied to many new physics models. The prospects of their effects at the CEPC are also examined assuming a 0.002 accuracy in the cross section measurement

Semileptonic BcB_{c} meson decays to S-wave charmonia and X(3872)X(3872) within the covariant light-front approach

In this work, we investigate the semileptonic decays of $B_{c}$ meson to $\eta_{c}(1S,2S,3S)$, $\psi(1S,2S,3S)$ and $X(3872)$ within the framework of covariant light-front quark model (CLFQM). We combine the helicity amplitudes via the corresponding form factors to obtain the branching ratios of the semileptonic decays $B_{c}\to \eta_{c}(1S, 2S, 3S)\ell\nu_{\ell}$, $B_{c}\to \psi(1S, 2S, 3S))\ell\nu_{\ell}$ and $B_{c}\to X(3872)\ell\nu_{\ell}$ with $\ell=e,\mu,\tau$. In view of the $R_{J/\Psi}$ anomaly released by the LHCb collaboration, it is necessary to calculate the ratios $R_X$ with $X=\psi(1S,2S,3S),\eta_c(1S,2S,3S),X(3872)$ systematically, which are helpful to check the lepton flavor universality (LFU). Furthermore, we also take into account another two physical observables, one is the longitudinal polarization fraction $f_{L}$ and the other is the forward-backward asymmetry $A_{FB}$, which can provide new clues to understand the $R_{J /\Psi}$ anomaly. Such theoretical predictions are necessary and interesting, which can be tested in the future LHCb experiments.Comment: 23 pages, 4 figure

Quasi-two-body decays Bc→K∗h→KπhB_c \to K^{*} h \to K \pi h in the perturbative QCD

In this work we study the quasi-two-body decays $B_c \to \ K^{*} h \to K \pi h (h = D, D_s, K, \pi, \eta, \eta')$ in the perturbative QCD (PQCD) approach. The two-meson distribution amplitudes (DAs) $\Phi^{\text{P-wave}}_{K\pi}$ are introduced to describe the final state interactions of the K \pi pair, which involve the time-like form factors F_{K\pi}(s) parameterized by the relativistic Breit-Wigner function and the Gegenbauer polynomials. We calculate the branching ratios for these quasi-two-body decays, from which one can obtain the branching raios for the corresponding two-body decays under the narrow width approximation relation. We find that $B^+_c\to K^{*+}D^0$ and $B^+_c\to K^{*0}D^+$ have the largest branching ratios, which can reach up to $10^{-6}$, while the branching ratios for other two-body decays are very small and only about $10^{-8}\sim10^{-7}$. As we expected that the branching ratios of the pure annihilation decays are usually small, while in our considered such type of decays, the channel $B_c^+ \to \bar K^{*0}K^{+}$ has the largest branching ratio, which is near $10^{-6}$. These results are consistent with the previously PQCD calculations obtained in the two-body framework, which can be tested by the future LHCb experiments. For the decays $B_c^+ \to K^{*+} D^{0}\to K^{0}\pi^+D^{0} , B_c^+ \to K^{*0}D^{+}\to K^{+}\pi^-D^{+}$ and $B_c^+ \to \bar K^{*0}D_s^{+}\to K^{-}\pi^+D_s^{+}$, we calculate their direct CP violations and find that $A_{CP}(B_c^+ \to K^{*+}D^{0}\to K^{0}\pi^+D^{0})=(-14.6_{-1.12}^{+9.19})\%$ is the largest one, which is possible measured by the present LHCb experiments. For the pure annihilation type decays, there is no CP violations because only the tree operators are involved. Furthermore, we also give the differential distributions of the branching ratios and the direct CP violations for the decays $B_c\to K^* D_{(s)}\to K \pi D_{(s)}$.Comment: 15 pages, 3 figures, 2 table

HIF-1α Contributes to Hypoxia-induced Invasion and Metastasis of Esophageal Carcinoma via Inhibiting E-cadherin and Promoting MMP-2 Expression

Hypoxia-inducible factor-1α (HIF-1α) has been found to enhance tumor invasion and metastasis, but no study has reported its action in esophageal carcinoma. The goal of this study was to explore the probable mechanism of HIF-1α in the invasion and metastasis of esophageal carcinoma Eca109 cells in vitro and in vivo. mRNA and protein expression of HIF-1α, E-cadherin and matrix metalloproteinase-2 (MMP-2) under hypoxia were detected by RT-PCR and Western blotting. The effects of silencing HIF-1α on E-cadherin, MMP-2 mRNA and protein expression under hypoxia or normoxia were detected by RT-PCR and Western blotting, respectively. The invasive ability of Eca109 cells was tested using a transwell chambers. We established an Eca109-implanted tumor model and observed tumor growth and lymph node metastasis. The expression of HIF-1α, E-cadherin and MMP-2 in xenograft tumors was detected by Western blotting. After exposure to hypoxia, HIF-1α protein was up-regulated, both mRNA and protein levels of E-cadherin were down-regulated and MMP-2 was up-regulated, while HIF-1α mRNA showed no significant change. SiRNA could block HIF-1α effectively, increase E-cadherin expression and inhibit MMP-2 expression. The number of invading cells decreased after HIF-1α was silenced. Meanwhile, the tumor volume was much smaller, and the metastatic rate of lymph nodes and the positive rate were lower in vivo. Our observations suggest that HIF-1α inhibition might be an effective strategy to weaken invasion and metastasis in the esophageal carcinoma Eca109 cell line

Gene Expression Divergence and Evolutionary Analysis of the Drosomycin Gene Family in Drosophila melanogaster

Drosomycin (Drs) encoding an inducible 44-residue antifungal peptide is clustered with six additional genes, Dro1, Dro2, Dro3, Dro4, Dro5, and Dro6, forming a multigene family on the 3L chromosome arm in Drosophila melanogaster. To get further insight into the regulation of each member of the drosomycin gene family, here we investigated gene expression patterns of this family by either microbe-free injury or microbial challenges using real time RT-PCR. The results indicated that among the seven drosomycin genes, Drs, Dro2, Dro3, Dro4, and Dro5 showed constitutive expressions. Three out of five, Dro2, Dro3, and Dro5, were able to be upregulated by simple injury. Interestingly, Drs is an only gene strongly upregulated when Drosophila was infected with microbes. In contrast to these five genes, Dro1 and Dro6 were not transcribed at all in either noninfected or infected flies. Furthermore, by 5′ rapid amplification of cDNA ends, two transcription start sites were identified in Drs and Dro2, and one in Dro3, Dro4, and Dro5. In addition, NF-κB binding sites were found in promoter regions of Drs, Dro2, Dro3, and Dro5, indicating the importance of NF-κB binding sites for the inducibility of drosomycin genes. Based on the analyses of flanking sequences of each gene in D. melanogaster and phylogenetic relationship of drosomycins in D. melanogaster species-group, we concluded that gene duplications were involved in the formation of the drosomycin gene family. The possible evolutionary fates of drosomycin genes were discussed according to the combining analysis of gene expression pattern, gene structure, and functional divergence of these genes

catena-Poly[silver(I)-μ-acridine-9-carboxyl­ato-κ3 N:O,O′]

In the title coordination polymer, [Ag(C14H8NO2)]n, the AgI cation is coordinated by two O atoms and one N atom from two symmetry-related acridine-9-carboxyl­ate ligands in a distorted trigonal-planar geometry. The metal atoms are connected by the ligands to form chains running parallel to the b axis. π–π stacking inter­actions [centroid-to-centroid distances 3.757 (2)–3.820 (2) Å] and weak Ag⋯O inter­actions further link the chains to form a layer network parallel to the ab plane. The AgI cation is disordered over two positions, with refined site-occupancy factors of 0.73 (3):0.27 (3)

Effect of rosiglitazone on rabbit model of myocardial ischemia-reperfusion injury

AbstractObjectiveTo explore mechanism and protective effect of rosiglitazone on myocardial ischemia reperfusion (I/R) injury.MethodsA total of 48 male Japanese white big-ear rabbits were randomly divided into control group (A), I/R group (B), low dose of rosiglitazone group (C), high dose of rosiglitazone group (D). Plasma concentration of and also reduced the concentration of plasma serum creatine kinase (CK), CK-MB, high-sensitivity C-reactive protein (hsCRP), ultra-superoxide dismutase (SOD), malondialdehyde (MDA), lactic acid glutathione skin peroxidase (GSH-PX), nitric oxide (NO) and endothelin (ET) were measured 1 h later after I/R. Twenty-four hours after I/R the hearts were harvested for pathological and ultrastructural analysis. Area of myocardial infarction were tested.ResultsPlasma concentration of CK, CK-MB, hsCRP, NO, MDA and ET were decreased in C, D group compared with group B. Plasma concentration of T-SOD and GSH-Px were increased significantly in C, D group compared with group B. Compared with group B, pathological and ultrastructural changes in C and D group were slightly. There was significant difference in myocardial infarction area between group C, D and group B (P<0.05). Myocardial infarction area and arrhythmia rate were lower in group C, D compare with group B.ConclusionsRosiglitazone may protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration, inhibit inflammatory reaction, and improve endothelial function

catena-Poly[zinc(II)-bis­[μ2-3-(3-pyrid­yl)­benzoato]-κ2 O:N;κ2 N:O]

In the title compound, [Zn(C12H8NO2)2]n, the Zn2+ cation is coordinated by a pair of carboxyl­ate O atoms as well as two pyridyl N atoms to afford a distorted tetra­hedral environment. Adjacent Zn2+ cations, with a separation of 8.807 (2) Å, are linked by two 3-(3-pyrid­yl)benzoate ligand bridges, generating an infinite ribbon extending parallel to [001]

A case report of complete remission of acute myeloid leukemia combined with DNMT3A, FLT3-TKD, and IDH2 gene mutations and active pulmonary tuberculosis treated with homeharringtonine + venetoclax + azacytidine

In March 2022, a 58-year-old man was admitted to the local hospital for nausea and vomiting. His blood routine indicated that he had leukocytosis and anemia. The patient was diagnosed with acute myeloid leukemia (AML)-M5b accompanied by DNMT3A, FLT3-TKD, and IDH2 mutations, chest CT revealed pulmonary tuberculosis (TB). Acid-fast bacillus (AFB) was detected in sputum. The patient then received anti-TB treatment with isoniazid + rifampicin + pyrazinamide + ethambutol. On April 8, he was transferred to our hospital's Hematology Department after three consecutive negative sputum smears. He was administered the VA (Venetoclax + Azacytidine) regimen of anti-leukemia treatment and also received levofloxacin + isohydrazide + pyrazinamide + ethambutol anti-TB treatment. After one course of VA therapy, there was no remission in the bone marrow. Therefore, the patient received the HVA (Homeharringtonine + Venetoclax + Azacytidine) regimen of anti-leukemia treatment. On May 25, the bone marrow smear revealed that the original mononuclear cells were 1%. Moreover, bone marrow flow cytometry revealed the absence of any abnormal cells. mNGS showed DNMT3A (mutation rate 44.7%), but no mutations were detected in FLT3-TKD and IDH2. The patient then received the HVA regimen three consecutive times, resulting in complete remission. Repeated chest CT examinations revealed progressive regression of pulmonary TB foci, no AFB was detected in the sputum. This AML patient with DNMT3A, FLT3-TKD, and IDH2 mutations and active TB is difficult to treat. It is very necessary for him to administer prompt anti-leukemia treatment under the premise of active anti-TB treatment. The HVA regimen is effective for this patient