Transport model study of nuclear stopping in heavy ion collisions over an energy range from 0.09A GeV to 160A GeV

Nuclear stopping in the heavy ion collisions over a beam energy range from SIS, AGS up to SPS is studied in the framework of the modified UrQMD transport model, in which mean field potentials of both formed and "pre-formed" hadrons (from string fragmentation) and medium modified nucleon-nucleon elastic cross sections are considered. It is found that the nuclear stopping is influenced by both the stiffness of the equation of state and the medium modifications of nucleon-nucleon cross sections at SIS energies. At the high SPS energies, the two-bump structure is shown in the experimental rapidity distribution of free protons, which can be understood with the consideration of the "pre-formed" hadron potentials.Comment: 15 pages, 7 figure

A Rho family GTPase controls actin dynamics and tip growth via two counteracting downstream pathways in pollen tubes.

Tip growth in neuronal cells, plant cells, and fungal hyphae is known to require tip-localized Rho GTPase, calcium, and filamentous actin (F-actin), but how they interact with each other is unclear. The pollen tube is an exciting model to study spatiotemporal regulation of tip growth and F-actin dynamics. An Arabidopsis thaliana Rho family GTPase, ROP1, controls pollen tube growth by regulating apical F-actin dynamics. This paper shows that ROP1 activates two counteracting pathways involving the direct targets of tip-localized ROP1: RIC3 and RIC4. RIC4 promotes F-actin assembly, whereas RIC3 activates Ca(2+) signaling that leads to F-actin disassembly. Overproduction or depletion of either RIC4 or RIC3 causes tip growth defects that are rescued by overproduction or depletion of RIC3 or RIC4, respectively. Thus, ROP1 controls actin dynamics and tip growth through a check and balance between the two pathways. The dual and antagonistic roles of this GTPase may provide a unifying mechanism by which Rho modulates various processes dependent on actin dynamics in eukaryotic cells

Solving the mystery of human sleep schedules one mutation at a time.

Sleep behavior remains one of the most enigmatic areas of life. The unanswered questions range from "why do we sleep?" to "how we can improve sleep in today's society?" Identification of mutations responsible for altered circadian regulation of human sleep lead to unique opportunities for probing these territories. In this review, we summarize causative circadian mutations found from familial genetic studies to date. We also describe how these mutations mechanistically affect circadian function and lead to altered sleep behaviors, including shifted or shortening of sleep patterns. In addition, we discuss how the investigation of mutations can not only expand our understanding of the molecular mechanisms regulating the circadian clock and sleep duration, but also bridge the pathways between clock/sleep and other human physiological conditions and ailments such as metabolic regulation and migraine headaches

Episodic neurologic disorders: syndromes, genes, and mechanisms.

Many neurologic diseases cause discrete episodic impairment in contrast with progressive deterioration. The symptoms of these episodic disorders exhibit striking variety. Herein we review what is known of the phenotypes, genetics, and pathophysiology of episodic neurologic disorders. Of these, most are genetically complex, with unknown or polygenic inheritance. In contrast, a fascinating panoply of episodic disorders exhibit Mendelian inheritance. We classify episodic Mendelian disorders according to the primary neuroanatomical location affected: skeletal muscle, cardiac muscle, neuromuscular junction, peripheral nerve, or central nervous system (CNS). Most known Mendelian mutations alter genes that encode membrane-bound ion channels. These mutations cause ion channel dysfunction, which ultimately leads to altered membrane excitability as manifested by episodic disease. Other Mendelian disease genes encode proteins essential for ion channel trafficking or stability. These observations have cemented the channelopathy paradigm, in which episodic disorders are conceptualized as disorders of ion channels. However, we expand on this paradigm to propose that dysfunction at the synaptic and neuronal circuit levels may underlie some episodic neurologic entities

Blow-up solutions and peakons to a generalized μ\mu-Camassa-Holm integrable equation

Consideration here is a generalized $\mu$-type integrable equation, which can be regarded as a generalization to both the $\mu$-Camassa-Holm and modified $\mu$-Camassa-Holm equations. It is shown that the proposed equation is formally integrable with the Lax-pair and the bi-Hamiltonian structure and its scale limit is an integrable model of hydrodynamical systems describing short capillary-gravity waves. Local well-posedness of the Cauchy problem in the suitable Sobolev space is established by the viscosity method. Existence of peaked traveling-wave solutions and formation of singularities of solutions for the equation are investigated. It is found that the equation admits a single peaked soliton and multi-peakon solutions. The effects of varying $\mu$-Camassa-Holm and modified $\mu$-Camassa-Holm nonlocal nonlinearities on blow-up criteria and wave breaking are illustrated in detail. Our analysis relies on the method of characteristics and conserved quantities and is proceeded with a priori differential estimates.Comment: 36 page