Implications of the Little Higgs Dark Matter and T-odd Fermions

We study the phenomenology of dark matter in the Littlest Higgs model with T-parity after the discovery of Higgs boson. We analyze the relic abundance of dark matter, focusing on the effects of coannihilaitons with T-odd fermions. After determining the parameter space that predicts the correct relic abundance measured by WMAP and Planck collaborations, we evaluate the elastic scattering cross section between dark matter and nucleon. In comparison with experimental results, we find that the lower mass of dark matter is constrained mildly by LUX 2013 while the future XENON experiment has potential to explore most of the parameter space for both T-odd lepton and T-odd quark coannihilation scenarios. We also study the collider signatures of T-odd fermion pair production at the LHC. Even though the production cross sections are large, it turns out very challenging to search for these T-odd fermions directly at the collider because the visible charged leptons or jets are very soft. Furthermore, we show that, with an extra hard jet radiated out from the initial state, the T-odd quark pair production can contribute significantly to mono-jet plus missing energy search at the LHC

Constraints on Unparticle Interactions from Invisible Decays of Z, Quarkonia and Neutrinos

Unparticles (\U) interact weakly with particles. The direct signature of unparticles will be in the form of missing energy. We study constraints on unparticle interactions using totally invisible decay modes of $Z$, vector quarkonia $V$ and neutrinos. The constraints on the unparticle interaction scale \Lambda_\U are very sensitive to the dimension d_\U of the unparticles. From invisible $Z$ and $V$ decays, we find that with d_\U close to 1 for vector \U, the unparticle scale \Lambda_\U can be more than $10^4$ TeV, and for d_\U around 2, the scale can be lower than one TeV. From invisible neutrino decays, we find that if d_\U is close to 3/2, the scale can be more than the Planck mass, but with d_\U around 2 the scale can be as low as a few hundred GeV. We also study the possibility of using V (Z)\to \gamma + \U to constrain unparticle interactions, and find that present data give weak constraints.Comment: 12 pages, 4 figures, version to appear in JHEP

Arachnoid Cyst Presenting With Sudden Hearing Loss

Arachnoid cysts can occur at different intracranial sites, including the cerebellopontine angle (CPA). They often occur in childhood, in the posterior fossa. They may present with symptoms such as dizziness, tinnitus and hearing loss, or they may be asymptomatic. Presentation with sudden deafness is very rare. We report the unusual presentation of a 67-year-old male with CPA arachnoid cyst and the complaint of sudden-onset deafness. In this case, the cystic lesion at the CPA was found by magnetic resonance imaging of the brain. Pathology after retromastoid suboccipital craniotomy confirmed an arachnoid cyst. The treatment of this patient is discussed and the possible causes of CPA arachnoid cyst are briefly reviewed

The sequence of the CA-SP1 junction accounts for the differential sensitivity of HIV-1 and SIV to the small molecule maturation inhibitor 3-O-{3',3'-dimethylsuccinyl}-betulinic acid

BACKGROUND: Despite the effectiveness of currently available antiretroviral therapies in the treatment of HIV-1 infection, a continuing need exists for novel compounds that can be used in combination with existing drugs to slow the emergence of drug-resistant viruses. We previously reported that the small molecule 3-O-{3',3'-dimethylsuccinyl}-betulinic acid (DSB) specifically inhibits HIV-1 replication by delaying the processing of the CA-SP1 junction in Pr55(Gag). By contrast, SIVmac239 replicates efficiently in the presence of high concentrations of DSB. To determine whether sequence differences in the CA-SP1 junction can fully account for the differential sensitivity of HIV-1 and SIV to DSB, we engineered mutations in this region of two viruses and tested their sensitivity to DSB in replication assays using activated human primary CD4(+ )T cells. RESULTS: Substitution of the P2 and P1 residues of HIV-1 by the corresponding amino acids of SIV resulted in strong resistance to DSB, but the mutant virus replicated with reduced efficiency. Conversely, replication of an SIV mutant containing three amino acid substitutions in the CA-SP1 cleavage site was highly sensitive to DSB, and the mutations resulted in delayed cleavage of the CA-SP1 junction in the presence of the drug. CONCLUSIONS: These results demonstrate that the CA-SP1 junction in Pr55(Gag )represents the primary viral target of DSB. They further suggest that the therapeutic application of DSB will be accompanied by emergence of mutant viruses that are highly resistant to the drug but which exhibit reduced fitness relative to wild type HIV-1

An Elusive Vector Dark Matter

Even though the sensitivity of direct dark matter search experiments reach the level about $10^{-45}~{\rm cm}^2$, there is no confident signal of dark matter been observed. We point out that, if dark matter is a vector boson, the null result in direct dark matter search experiments may due to the destructive effects in dark-matter-nucleon elastic scattering. We illustrate the scenario using a modified Higgs portal model that includes exotic quarks. The significant cancellation can occur for certain mass gap between heavy quark and dark matter. As a result, the spin-independent dark-matter-nucleon elastic scattering is so suppressed that the future direct search experiments can hardly observe the signal of dark matter.Comment: 11 pages, 5 figure

Using Adaptive Structuraction Theory to Study the Implementation of CIM Systems: A case study of TFT-LCD Companies

CIM (Computer Integrated Manufacturing) is like a strategic weapon that helps industries increase their capacity for competing. Case study by interviewing enterprise is the main technique applied in this research. Base on AST (Adaptive Structuraction Theory) introduced by multiple case analyses, in the process of implementing CIM the interaction between CIM and organization of two TFT-LCD industries whose business operation characteristics are different will be discussed. The research result can be treated as a reference for enterprises to perform their CIM system more effectively and promote their core competency. In the paper, some discoveries are found as follows: the enterprises that have higher degree of automation always pay more attention to the operation standard of manufacturing and system, and consider the correspondence between them for need of process automation. On the other hand, the enterprises that have lower degree of automation always pay more attention to the rationalization of production lines, the convenience of adjusting operation process after the system is implemented, division of labor among the related organizations and their responsibility as well. The reason why causes the difference is the former thinks both the system functions and information linking techniques are two most important key points in the CIM project, so the employee rate of the staff related with IT must be increased in the project organization

Mechanism of action and resistant profile of anti-HIV-1 coumarin derivatives

Dicamphanoyl khellactone (DCK) is a coumarin derivative that can potently inhibit HIV-1 replication. DCK does not inhibit RNA-dependent DNA synthesis. However, an HIV reverse transcriptase (RT) inhibitor-resistant strain, HIV-1/RTMDR1, is resistant to DCK. Thus, it is possible that HIV-1 RT is the target of DCK. To test this possibility, DCK-resistant viruses were selected in the presence of DCK. Our results indicate that a single amino acid mutation, E138K in HIV-1 RT, is sufficient to confer DCK resistance. Interestingly, a DCK derivative, 3'R,4'R-Di-O-(-)-camphanoyl-2-ethyl-2',2'-dimethyldihydropyrano[2,3-f]chromo ne (DCP8), is effective against HIV-1/RTMDR1. However, the DCK-escape virus carrying the E138K mutation remains resistant to DCP8. Since DCK did not inhibit the RNA-dependent DNA polymerase activity of HIV-1 RT when using poly-rA or poly-rC as template, we evaluated the effect of DCK on the DNA-dependent DNA polymerase activity of HIV-1 RT. Our results indicate that DCK can inhibit the DNA-dependent DNA polymerase activity of HIV-1 RT. In conclusion, DCK is a unique HIV-1 RT inhibitor that inhibits the DNA-dependent DNA polymerase activity. In contrast, DCK did not significantly affect the RNA-dependent DNA polymerase activity when poly-rA or poly-rC was used as templates. An E138K mutation in the non-nucleoside RT inhibitors (NNRTIs) binding pocket of HIV-1 RT confers resistance to DCK and its chromone derivative, DCP8

Picomolar Dichotomous Activity of Gnidimacrin Against HIV-1

Highly active antiretroviral therapy (HAART) has offered a promising approach for controlling HIV-1 replication in infected individuals. However, with HARRT, HIV-1 is suppressed rather than eradicated due to persistence of HIV-1 in latent viral reservoirs. Thus, purging the virus from latent reservoirs is an important strategy toward eradicating HIV-1 infection. In this study, we discovered that the daphnane diterpene gnidimacrin, which was previously reported to have potent anti-cancer cell activity, activated HIV-1 replication and killed persistently-infected cells at picomolar concentrations. In addition to its potential to purge HIV-1 from latently infected cells, gnidimacrin potently inhibited a panel of HIV-1 R5 virus infection of peripheral blood mononuclear cells (PBMCs) at an average concentration lower than 10 pM. In contrast, gnidimacrin only partially inhibited HIV-1 ×4 virus infection of PBMCs. The strong anti-HIV-1 R5 virus activity of gnidimacrin was correlated with its effect on down-regulation of the HIV-1 coreceptor CCR5. The anti-R5 virus activity of gnidimacrin was completely abrogated by a selective protein kinase C beta inhibitor enzastaurin, which suggests that protein kinase C beta plays a key role in the potent anti-HIV-1 activity of gnidimacrin in PBMCs. In summary, these results suggest that gnidimacrin could activate latent HIV-1, specifically kill HIV-1 persistently infected cells, and inhibit R5 viruses at picomolar concentrations