Three-Wave Backward Optical Solitons

Three-wave solitons backward propagating with respect to a pump wave are generated in nonlinear optical media through stimulated Brillouin scattering (SBS) in optical fibers or through the non-degenerate three-wave interaction in quadratic (χ (2) ) nonlinear media. In an optical fiber-ring cavity, nanosecond solitary wave morphogenesis takes place when it is pumped with a continuous wave (c.w.). A backward dissipative Stokes soliton is generated from the hypersound waves stimulated by electrostriction between the forward pump wave and the counterpropagating Stokes wave. Superluminous and subluminous dissipative solitons are controlled via a single parameter: the feedback or reinjection for a given pump intensity or the pump intensity for a given feedback. In a c.w. pumped optical parametric oscillator (OPO), backward picosecond soliton generation takes place for non-degenerate three-wave interaction in the quadratic medium. The resonant condition is automatically satisfied in stimulated Brillouin backscattering when the fiber-ring laser contains a large number of longitudinal modes beneath the Brillouin gain curve. However, in order to achieve quasiphase matching between the three optical waves (the forward pump wave and the backwar

Genetic and Neurophysiological Correlates of the Age of Onset of Alcohol Use Disorders in Adolescents and Young Adults

Discrete time survival analysis (DTSA) was used to assess the age-specific association of event related oscillations (EROs) and CHRM2 gene variants on the onset of regular alcohol use and alcohol dependence. The subjects were 2938 adolescents and young adults ages 12 to 25. Results showed that the CHRM2 gene variants and ERO risk factors had hazards which varied considerably with age. The bulk of the significant age-specific associations occurred in those whose age of onset was under 16. These associations were concentrated in those subjects who at some time took an illicit drug. These results are consistent with studies which associate greater rates of alcohol dependence among those who begin drinking at an early age. The age specificity of the genetic and neurophysiological factors is consistent with recent studies of adolescent brain development, which locate an interval of heightened vulnerability to substance use disorders in the early to mid teens

Curcumin and Cancer Cells: How Many Ways Can Curry Kill Tumor Cells Selectively?

Cancer is a hyperproliferative disorder that is usually treated by chemotherapeutic agents that are toxic not only to tumor cells but also to normal cells, so these agents produce major side effects. In addition, these agents are highly expensive and thus not affordable for most. Moreover, such agents cannot be used for cancer prevention. Traditional medicines are generally free of the deleterious side effects and usually inexpensive. Curcumin, a component of turmeric (Curcuma longa), is one such agent that is safe, affordable, and efficacious. How curcumin kills tumor cells is the focus of this review. We show that curcumin modulates growth of tumor cells through regulation of multiple cell signaling pathways including cell proliferation pathway (cyclin D1, c-myc), cell survival pathway (Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1), caspase activation pathway (caspase-8, 3, 9), tumor suppressor pathway (p53, p21) death receptor pathway (DR4, DR5), mitochondrial pathways, and protein kinase pathway (JNK, Akt, and AMPK). How curcumin selectively kills tumor cells, and not normal cells, is also described in detail