Functional diversity of chemokines and chemokine receptors in response to viral infection of the central nervous system.

Encounters with neurotropic viruses result in varied outcomes ranging from encephalitis, paralytic poliomyelitis or other serious consequences to relatively benign infection. One of the principal factors that control the outcome of infection is the localized tissue response and subsequent immune response directed against the invading toxic agent. It is the role of the immune system to contain and control the spread of virus infection in the central nervous system (CNS), and paradoxically, this response may also be pathologic. Chemokines are potent proinflammatory molecules whose expression within virally infected tissues is often associated with protection and/or pathology which correlates with migration and accumulation of immune cells. Indeed, studies with a neurotropic murine coronavirus, mouse hepatitis virus (MHV), have provided important insight into the functional roles of chemokines and chemokine receptors in participating in various aspects of host defense as well as disease development within the CNS. This chapter will highlight recent discoveries that have provided insight into the diverse biologic roles of chemokines and their receptors in coordinating immune responses following viral infection of the CNS

Polymorphism of the catechol-O-methyltransferase gene in Han Chinese patients with psoriasis vulgaris

Psoriasis vulgaris is defined by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils and other types of leukocytes in the affected skin. Catechol-O-methyltransferase (COMT) 158 polymorphism can reduce the activity of the COMT enzyme that may trigger defective differentiation of keratinocytes in psoriasis. Immunocytes can degrade and inactivate catecholamines via monamine oxidase (MAO) and COMT in the cells. We hypothesized that the COMT-158G > A polymorphism was associated with the risk of psoriasis vulgaris in Han Chinese people. In a hospital-based case-control study, 524 patients with psoriasis vulgaris and 549 psoriasis-free controls were studied. COMT-158 G > A polymorphism was genotyped using the PCR sequence-specific primer (PCR-SSP) technique. We found no statistically significant association between the COMT-158 allele A and the risk of psoriasis vulgaris (p = 0.739 adjusted OR = 1.03; 95% CI = 0.81-1.31). This suggests that the COMT-158 G > A polymorphism may not contribute to the etiology of psoriasis vulgaris in the Han Chinese population

Measurement of the time-dependent CP asymmetries in B0s → J/ψK0S

The first measurement of decay-time-dependent CP asymmetries in the decay B0s → J/ψK0S and an updated measurement of the ratio of branching fractions B(B0s→J/ψK0S)/B(B0→J/ψK0S)are presented. The results are obtained using data corresponding to an integrated luminosity of 3.0 fb−1 of proton-proton collisions recorded with the LHCb detector at centre-of-mass energies of 7 and 8TeV. The results on the CP asymmetries are Aat B(B0s→J/ψK0S)= 0.49 ±0.77 0.65 (stat) ± 0.06(syst) , Cdir(B0s→J/ψK0S)= −0.28 ± 0.41(stat) ± 0.08(syst) , Smix(B0s→J/ψK0S)= −0.08 ± 0.40(stat) ± 0.08(syst) . The ratio B (B0s→J/ψK0S)= / B(B0s→J/ψK0S)= is measured to be 0.0431 ± 0.0017(stat) ± 0.0012(syst) ± 0.0025(fs/fd) , where the last uncertainty is due to the knowledge of the B0 s and B0 production fractions.S