On the Unitarity Triangles of the CKM Matrix

The unitarity triangles of the $3\times 3$ Cabibbo-Kobayashi-Maskawa (CKM) matrix are studied in a systematic way. We show that the phases of the nine CKM rephasing invariants are indeed the outer angles of the six unitarity triangles and measurable in the $CP$-violating decay modes of $B_{d}$ and $B_{s}$ mesons. An economical notation system is introduced for describing properties of the unitarity triangles. To test unitarity of the CKM matrix we present some approximate but useful relations among the sides and angles of the unitarity triangles, which can be confronted with the accessible experiments of quark mixing and $CP$ violation.Comment: 9 Latex pages; LMU-07/94 and PVAMU-HEP-94-5 (A few minor changes are made, accepted for publication in Phys. Lett. B

CP symmetry and fermion masses in O(10) grand unification models

O(10) grand unification models which do not necessarily have an extra global symmetry are discussed, taking the model with one 10-plet in the Yukawa sector as an example. A strong correlation between mass ratios and CP is found. The mass relation $m_t/m_b=v_u/v_d$ is recovered when $G_W=0$; and another special relation $m_t/m_b=G_E/G_W$ appears when $v_d=0$, where $G_{E,W}$ are Yukawa coupling constants and $v_{u,d}$ are VEVs. To facilitate this discussion, a set of $O(10)$ $\gamma$- matrices is offered based on a physical representation of the spinors and that of the vector of the $SO(10)$ group. Flavor changing neutral currents in such models are also discussed.Comment: 17 pages, Latex fil

Magmatic record of India-Asia collision

This work was financially co-supported by Chinese Academy of Sciences (XDB03010301) and other Chinese funding agencies (Project 973: 2011CB403102 and 2015CB452604; NSFC projects: 41225006, 41273044, and 41472061).New geochronological and geochemical data on magmatic activity from the India-Asia collision zone enables recognition of a distinct magmatic flare-up event that we ascribe to slab breakoff. This tie-point in the collisional record can be used to back-date to the time of initial impingement of the Indian continent with the Asian margin. Continental arc magmatism in southern Tibet during 80-40 Ma migrated from south to north and then back to south with significant mantle input at 70-43 Ma. A pronounced flare up in magmatic intensity (including ignimbrite and mafic rock) at ca. 52-51 Ma corresponds to a sudden decrease in the India-Asia convergence rate. Geological and geochemical data are consistent with mantle input controlled by slab rollback from ca. 70 Ma and slab breakoff at ca. 53 Ma. We propose that the slowdown of the Indian plate at ca. 51 Ma is largely the consequence of slab breakoff of the subducting Neo-Tethyan oceanic lithosphere, rather than the onset of the India-Asia collision as traditionally interpreted, implying that the initial India-Asia collision commenced earlier, likely at ca. 55 Ma.Publisher PDFPeer reviewe

Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

<p>Abstract</p> <p>Background</p> <p>To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.</p> <p>Methods</p> <p>MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR.</p> <p>Results</p> <p>HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased.</p> <p>Conclusions</p> <p>Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.</p