Finding the Right Fit: A Comparison of Process Assumptions Underlying Popular Drift-Diffusion Models

Recent research makes increasing use of eye-tracking methodologies to generate and test process models. Overall, such research suggests that attention, generally indexed by fixations (gaze duration), plays a critical role in the construction of preference, although the methods employed to support this supposition differ substantially. In two studies we empirically test prototypical versions of prominent processing assumptions against one another and several base models. We find that general evidence accumulation processes provide a good fit to the data. An accumulation process that assumes leakage and temporal variability in evidence weighting (i.e. a primacy effect) fits the aggregate data, both in terms of choices and decision times, and does so across varying types of choices (e.g., charitable giving and hedonic consumption) and numbers of options well. However, when comparing models on the level of the individual, for a majority of participants simpler models capture choice data better. The theoretical and practical implications of these findings are discussed

The Striking Flower-in-Flower Phenotype of Arabidopsis thaliana Nossen (No-0) is Caused by a Novel LEAFY Allele

The transition to reproduction is a crucial step in the life cycle of any organism. In Arabidopsis thaliana the establishment of reproductive growth can be divided into two phases: Firstly, cauline leaves with axillary meristems are formed and internode elongation begins. Secondly, lateral meristems develop into flowers with defined organs. Floral shoots are usually determinate and suppress the development of lateral shoots. Here, we describe a transposon insertion mutant in the Nossen accession with defects in floral development and growth. Most strikingly is the outgrowth of stems from the axillary bracts of the primary flower carrying secondary flowers. Therefore, we named this mutant flower-in-flower (fif). However, the transposon insertion in the annotated gene is not the cause for the fif phenotype. By means of classical and genome sequencing-based mapping, the mutation responsible for the fif phenotype was found to be in the LEAFY gene. The mutation, a G-to-A exchange in the second exon of LEAFY, creates a novel lfy allele and results in a cysteine-to-tyrosine exchange in the α1-helix of LEAFY’s DNA-binding domain. This exchange abolishes target DNA-binding, whereas subcellular localization and homomerization are not affected. To explain the strong fif phenotype against these molecular findings, several hypotheses are discussed

Application of realistic effective interactions to the structure of the Zr isotopes

We calculate the low-lying spectra of the zirconium isotopes Z=40 with neutron numbers from N=52 to N=60 using the 1p1/20g9/2 proton and 2s1d0g7/20h11/2 neutron sub-shells to define the model space. Effective proton-proton, neutron--neutron and proton-neutron interactions have been derived using 88Sr as closed core and employing perturbative many-body techniques. The starting point is the nucleon-nucleon potential derived from modern meson exchange models. The comprehensive shell-model calculation performed in this work provides a qualitative reproduction of essential properties such as the sub-shell closures in 96Zr and 98Zr.Comment: To appear in Phys Rev C, june 2000, 8 figs, Revtex latex styl

ARHGEF7 (BETA-PIX) Acts as Guanine Nucleotide Exchange Factor for Leucine-Rich Repeat Kinase 2

Background: Mutations within the leucine-rich repeat kinase 2 (LRRK2) gene are a common cause of familial and sporadic Parkinson’s disease. The multidomain protein LRRK2 exhibits overall low GTPase and kinase activity in vitro. Methodology/Principal Findings: Here, we show that the rho guanine nucleotide exchange factor ARHGEF7 and the small GTPase CDC42 are interacting with LRRK2 in vitro and in vivo. GTPase activity of full-length LRRK2 increases in the presence of recombinant ARHGEF7. Interestingly, LRRK2 phosphorylates ARHGEF7 in vitro at previously unknown phosphorylation sites. We provide evidence that ARHGEF7 might act as a guanine nucleotide exchange factor for LRRK2 and that R1441C mutant LRRK2 with reduced GTP hydrolysis activity also shows reduced binding to ARHGEF7. Conclusions/Significance: Downstream effects of phosphorylation of ARHGEF7 through LRRK2 could be (i) a feedback control mechanism for LRRK2 activity as well as (ii) an impact of LRRK2 on actin cytoskeleton regulation. A newly identified familial mutation N1437S, localized within the GTPase domain of LRRK2, further underlines the importance of the GTPas

The Relationship of Visceral Adipose Tissue with Markers of Energy Homeostasis Following Weight-Loss

Excess levels of adipose tissue, in particular visceral adipose tissue (VAT), is closely associated with the metabolic syndrome and dysregulation of energy homeostasis. It is hypothesized that leptin resistance results in overconsumption of calories and reduced satiety. Recently, brain derived neurotrophic factor (BDNF), beyond functioning in learning and memory, is shown to play a role in energy homeostasis via its positive satiety effects on the hypothalamus. However, it remains to be elucidated how changes in visceral adipose tissue are associated with changes in circulating leptin and BDNF after weight-loss. PURPOSE: To identify changes in adiposity and circulating leptin and BDNF following a 3-month weight-loss program. METHODS: Sixty-five obese (mean±SEM; age=47.9±1.1 years; BMI=34.5±0.8 kg/m2;), men and women completed a 3-month weight-loss program that consisted of a reduced energy intake of 1200-1500 kcals/day using a high-volume low-calorie diet combined with a progressive walking program to target 300 min/wk. Fasted (12 hr) blood samples were collected at baseline and post-weight-loss (3 months) and assayed for concentrations of glucose, insulin, BDNF, and leptin. Using DXA, total VAT and subcutaneous (SubQ) adipose tissue mass were measured at baseline and post-weight-loss (3 months). To identify significant changes over time, ANOVA with repeated measures was performed with significance set at p\u3c0.05. RESULTS: Following the 3-month weight-loss program, both BMI and HOMA-IR were significantly reduced 9.3% and 49%, respectively. The reduction in BMI and HOMA-IR were matched by a significant reduction in both VAT (-658 g; -33%, p\u3c0.001) and SubQ (-367 g; -17%, p\u3c0.001). Interestingly, leptin was reduced and BDNF was increased by 43% (p\u3c0.001) and 42% (p=0.011), respectively. Linear regression revealed that changes in VAT were associated with changes in leptin (b=0.298, p=0.026), but not with BDNF (b=0.027, p=0.896). CONCLUSION: This study shows that the reduction in VAT, by caloric restriction and physical activity, was associated with the reduction in circulating leptin concentrations, but not with changes in BDNF. Changes in leptin and BDNF may be in part responsible for the normalization of the energy homeostasis observed after weight-loss; however, changes in BDNF may be independent of VAT

Microscopic shell-model description of the exotic nucleus ^{16}C

The structure of the neutron-rich carbon nucleus ^{16}C is described by introducing a new microscopic shell model of no-core type. The model space is composed of the 0s, 0p, 1s0d, and 1p0f shells. The effective interaction is microscopically derived from the CD-Bonn potential and the Coulomb force through a unitary transformation theory. Calculated low-lying energy levels of ^{16}C agree well with the experiment. The B(E2;2_{1}^{+} \to 0_{1}^{+}) value is calculated with the bare charges. The anomalously hindered B(E2) value for ^{16}C, measured recently, is well reproduced.Comment: 14 pages, 4 figures, considerable results and discussion are added, but the main conclusion is unchanged, accepted for publication in Phys. Lett.

LRRK2 transport is regulated by its novel interacting partner Rab32

Leucine-rich repeat kinase 2 (LRRK2) is a multi-domain 280 kDa protein that is linked to Parkinson's disease (PD). Mutations especially in the GTPase and kinase domains of LRRK2 are the most common causes of heritable PD and are also found in sporadic forms of PD. Although the cellular function of LRRK2 is largely unknown there is increasing evidence that these mutations cause cell death due to autophagic dysfunction and mitochondrial damage. Here, we demonstrate a novel mechanism of LRRK2 binding and transport, which involves the small GTPases Rab32 and Rab38. Rab32 and its closest homologue Rab38 are known to organize the trans-Golgi network and transport of key enzymes in melanogenesis, whereas their function in non-melanogenic cells is still not well understood. Cellular processes such as autophagy, mitochondrial dynamics, phagocytosis or inflammatory processes in the brain have previously been linked to Rab32. Here, we demonstrate that Rab32 and Rab38, but no other GTPase tested, directly interact with LRRK2. GFP-Trap analyses confirmed the interaction of Rab32 with the endogenous LRRK2. In yeast two-hybrid experiments we identified a predicted coiled-coil motif containing region within the aminoterminus of LRRK2 as the possible interacting domain. Fluorescence microscopy demonstrated a co-localization of Rab32 and LRRK2 at recycling endosomes and transport vesicles, while overexpression of a constitutively active mutant of Rab32 led to an increased co-localization with Rab7/9 positive perinuclear late endosomes/MVBs. Subcellular fractionation experiments supported the novel role of Rab32 in LRRK2 late endosomal transport and sorting in the cell. Thus, Rab32 may regulate the physiological functions of LRRK2

Signal Transduction Protein Array Analysis Links LRRK2 to Ste20 Kinases and PKC Zeta That Modulate Neuronal Plasticity

substrate phosphorylation..Ste20 kinases and PKC zeta contribute to neuronal Tau phosphorylation, neurite outgrowth and synaptic plasticity under physiological conditions. Our data suggest that these kinases may also be involved in synaptic dysfunction and neurite fragmentation in transgenic mice and in human PD patients carrying toxic gain-of-function LRRK2 mutations

Gamow-Teller Strength in the Region of 100^{100}Sn

New calculations are presented for Gamow-Teller beta decay of nuclei near $^{100}$Sn. Essentially all of the $^{100}$Sn Gamow-Teller decay strength is predicted to go to a single state at an excitation energy of 1.8 MeV in $^{100}$In. The first calculations are presented for the decays of neighboring odd-even and odd-odd nuclei which show, in contrast to $^{100}$Sn, surprisingly complex and broad Gamow-Teller strength distributions. The results are compared to existing experimental data and the resulting hindrance factors are discussed.Comment: 12 pages (latex) and 2 figures available on reques