bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of Dot1 in the Response to Alkylating DNA Damage in Saccharomyces cerevisiae: Regulation of DNA Damage Tolerance by the Error-Prone Polymerases Polζ/Rev1
Authors: Conde Francisco , San-Segundo Pedro A 
Published: June 2008

Abstract
Maintenance of genomic integrity relies on a proper response to DNA injuries integrated by the DNA damage checkpoint; histone modifications play an important role in this response. Dot1 methylates lysine 79 of histone H3. In Saccharomyces cerevisiae, Dot1 is required for the meiotic recombination checkpoint as well as for chromatin silencing and the G1/S and intra-S DNA damage checkpoints in vegetative cells. Here, we report the analysis of the function of Dot1 in the response to alkylating damage. Unexpectedly, deletion of DOT1 results in increased resistance to the alkylating agent methyl methanesulfonate (MMS). This phenotype is independent of the dot1 silencing defect and does not result from reduced levels of DNA damage. Deletion of DOT1 partially or totally suppresses the MMS sensitivity of various DNA repair mutants (rad52, rad54, yku80, rad1, rad14, apn1, rad5, rad30). However, the rev1 dot1 and rev3 dot1 mutants show enhanced MMS sensitivity and dot1 does not attenuate the MMS sensitivity of rad52 rev3 or rad52 rev1. In addition, Rev3-dependent MMS-induced mutagenesis is increased in dot1 cells. We propose that Dot1 inhibits translesion synthesis (TLS) by Polζ/Rev1 and that the MMS resistance observed in the dot1 mutant results from the enhanced TLS activity.
The Nuclear Dbf2-Related Kinase COT1 and the Mitogen-Activated Protein Kinases MAK1 and MAK2 Genetically Interact to Regulate Filamentous Growth, Hyphal Fusion and Sexual Development in Neurospora crassa
Authors: Maerz Sabine , Ziv Carmit , Vogt Nico , Helmstaedt Kerstin , Cohen Nourit , Gorovits Rena , Yarden Oded , Seiler Stephan 
Published: June 2008

Abstract
Ndr kinases, such as Neurospora crassa COT1, are important for cell differentiation and polar morphogenesis, yet their input signals as well as their integration into a cellular signaling context are still elusive. Here, we identify the cot-1 suppressor gul-4 as mak-2 and show that mutants of the gul-4/mak-2 mitogen-activated protein (MAP) kinase pathway suppress cot-1 phenotypes along with a concomitant reduction in protein kinase A (PKA) activity. Furthermore, mak-2 pathway defects are partially overcome in a cot-1 background and are associated with increased MAK1 MAPK signaling. A comparative characterization of N. crassa MAPKs revealed that they act as three distinct modules during vegetative growth and asexual development. In addition, common functions of MAK1 and MAK2 signaling during maintenance of cell-wall integrity distinguished the two ERK-type pathways from the p38-type OS2 osmosensing pathway. In contrast to separate functions during vegetative growth, the concerted activity of the three MAPK pathways is essential for cell fusion and for the subsequent formation of multicellular structures that are required for sexual development. Taken together, our data indicate a functional link between COT1 and MAPK signaling in regulating filamentous growth, hyphal fusion, and sexual development.
Sequence Divergence Impedes Crossover More Than Noncrossover Events During Mitotic Gap Repair in Yeast
Authors: Welz-Voegele Caroline , Jinks-Robertson Sue 
Published: June 2008

AbstractHomologous recombination between dispersed repeated sequences is important in shaping eukaryotic genome structure, and such ectopic interactions are affected by repeat size and sequence identity. A transformation-based, gap-repair assay was used to examine the effect of 2% sequence divergence on the efficiency of mitotic double-strand break repair templated by chromosomal sequences in yeast. Because the repaired plasmid could either remain autonomous or integrate into the genome, the effect of sequence divergence on the crossover–noncrossover (CO–NCO) outcome was also examined. Finally, proteins important for regulating the CO–NCO outcome and for enforcing identity requirements during recombination were examined by transforming appropriate mutant strains. Results demonstrate that the basic CO–NCO outcome is regulated by the Rad1-Rad10 endonuclease and the Sgs1 and Srs2 helicases, that sequence divergence impedes CO to a much greater extent than NCO events, that an intact mismatch repair system is required for the discriminating identical and nonidentical repair templates, and that the Sgs1 and Srs2 helicases play additional, antirecombination roles when the interacting sequences are not identical.
The Use of Scenario-Based-Learning Interactive Software to Create Custom Virtual Laboratory Scenarios for Teaching Genetics
Authors: Breakey Kate M , Levin Daniel , Miller Ian , Hentges Kathryn E 
Published: June 2008

Abstract
Mutagenesis screens and analysis of mutant phenotypes are one of the most powerful approaches for the study of genetics. Yet genetics students often have difficulty understanding the experimental procedures and breeding crosses required in mutagenesis screens and linking mutant phenotypes to molecular defects. Performing these experiments themselves often aids students in understanding the methodology. However, there are limitations to performing genetics experiments in a student laboratory. For example, the generation time of laboratory model organisms is considerable, and a laboratory exercise that involves many rounds of breeding or analysis of many mutants is not often feasible. Additionally, the cost of running a laboratory practical, along with safety considerations for particular reagents or protocols, often dictates the experiments that students can perform. To provide an alternative to a traditional laboratory module, we have used Scenario-Based-Learning Interactive (SBLi) software to develop a virtual laboratory to support a second year undergraduate course entitled “Genetic Analysis.” This resource allows students to proceed through the steps of a genetics experiment, without the time, cost, or safety constraints of a traditional laboratory exercise.
Modifying the journal impact factor by fractional citation weighting: The audience factor
Authors: Zitt Michel , Small Henry 
Published: June 2008

AbstractA new approach to the field normalization of the classical journal impact factor is introduced. This approach, called the audience factor, takes into consideration the citing propensity of journals for a given cited journal, specifically, the mean number of references of each citing journal, and fractionally weights the citations from those citing journals. Hence, the audience factor is a variant of a fractional citation‐counting scheme, but computed on the citing journal rather than the citing article or disciplinary level, and, in contrast to other cited‐side normalization strategies, is focused on the behavior of the citing entities. A comparison with standard journal impact factors from Thomson Reuters shows a more diverse representation of fields within various quintiles of impact, significant movement in rankings for a number of individual journals, but nevertheless a high overall correlation with standard impact factors.
Group Intensive Family Training (GIFT) for preschoolers with autism spectrum disorders
Authors: Anan Ruth M. , Warner Lori J. , McGillivary Jamie E. , Chong Ivy M. , Hines Stefani J. 
Published: June 2008

AbstractEarly, intensive behavioral intervention is effective in treating children with autism spectrum disorders (ASDs), but can be cost prohibitive. Expenses may be defrayed if children can benefit from parents acting as therapists. This quantitative case series examines the efficacy of the Group Intensive Family Training (GIFT) program, a 12‐week (180 h, delivered 3 h each weekday) parent‐training for preschoolers with ASDs. Parents were individually mentored in the hands‐on application of behavior analytic techniques, implementing these skills in vivo within a group of six parent–child dyads. Seventy‐two parents and children (ages 25–68 months) with ASDs participated in this study. Children's cognitive and adaptive functioning was assessed before and after the intervention program. Analyses revealed average gains of eight standard score points on the Mullen Early Learning Composite and five standard score points on the Vineland Adaptive Behavior Composite after 12 weeks of treatment. Additionally, 14% and 11% of the children moved from the ‘impaired’ to ‘non‐impaired’ range on Mullen and Vineland composite scores, respectively. This preliminary investigation suggests that GIFT's behavioral, group parent‐training can lead to significant, yet cost‐ and time‐efficient gains for children with ASDs. Results must be interpreted with caution because of the absence of a control group. Copyright © 2008 John Wiley & Sons, Ltd.
Multiplex pathogen detection based on spatially addressable microarrays of barcoded resins
Authors: Blais David R. , Alvarez‐Puebla Ramon A. , Bravo‐Vasquez Juan P. , Fenniri Hicham , Pezacki John Paul 
Published: June 2008

AbstractSuspension microsphere immunoassays are rapidly gaining recognition in antigen identification and infectious disease biodetection due to their simplicity, versatility and high‐throughput multiplex screening. We demonstrate a multiplex assay based on antibody‐functionalized barcoded resins (BCRs) to identify pathogen antigens in complex biological fluids. The binding event of a particular antibody on given bead (fluorescence) and the identification of the specific pathogen agent (vibrational fingerprint of the bead) can be achieved in a dispersive Raman system by exciting the sample with two different laser lines. Anthrax protective antigen, Franciscella tularensis lipopolysaccharide and CD14 antigens were accurately identified and quantified in tetraplex assays with a detection limit of 1 ng/mL. The rapid, versatile and simple analysis enabled by the BCRs demonstrates their potential for multiplex antigen detection and identification in a reconfigurable microarray format.
Development of the human hypogastric nerve sheath with special reference to the topohistology between the nerve sheath and other prevertebral fascial structures
Authors: Kinugasa Yusuke , Niikura Hitoshi , Murakami Gen , Suzuki Daisuke , Saito Shuji , Tatsumi Haruyuki , Ishii Masayuki 
Published: June 2008

AbstractSemi‐serial sections from the lumbosacral region of nine fetuses (8–25 weeks gestation) were examined to clarify the lumbar prevertebral fascial arrangement. The prevertebral fasciae became evident after 12 weeks of age. After 20 weeks of age, the hypogastric nerve (HGN) was sandwiched by two fascial structures; the ventral fascia which seemed to correspond to the mesorectal fascia, whereas the dorsal fascia corresponded to the presacral fascia. These fasciae or the HGN sheaths extended laterally along the ventral aspects of the great vessels and associated lymph follicles. The ventral fascia is, to some extent, fused with the mesocolon descendens on the left side of the body. Notably, the lateral continuation of these two fasciae also sandwiches the left ureter, but not the right ureter, presumably due to modifications by the left‐sided fusion fascia. A hypothetical common sheath for the HGN and ureter (i.e., the ureterohypogastric or vesicohypogastric fascia) might thus be an oversimplification. Before retroperitoneal fixation, the morphology of the peritoneal recess along the mesocolon descendens and mesosigmoid suggested interindividual differences in location, shape, and size. Therefore, in adults the ease of surgical separation of the rectum and left‐sided colon from the HGN seems to depend on interindividual differences in the development of the embryonic peritoneal recess. On the caudal side of the second sacral segment, fascial structures were restricted along and around the HGN, pelvic splanchnic nerve, and pelvic plexus. The rectal lateral ligament thus seems to represent a kind of migration fascia formed by mechanical stress. Clin. Anat. 21:558–567, 2008. © 2008 Wiley‐Liss, Inc.
An educational tool for controlling of SRM
Authors: Yigit Tuncay , Elmas Cetin 
Published: June 2008

AbstractThis article introduces an educational tool for a switched reluctance motor (SRM) drive system. It is prepared for undergraduate and graduate level students. Classical PI and Genetic PI controllers are used in SRM drive system. The Genetic PI controller was applied to the speed loop, replacing the classical PI controller. The tool software was implemented using C++ Builder on a PC. It has flexible structure and graphical interface. The students can be easily establishing a thorough understanding of both classical PI and genetic PI controller for a SRM drive system. The education tool allowed the student to interact with the SRM drive system and it is using controllers. Then it is responses on a dynamic and instantaneous basis under different operating conditions. © 2008 Wiley Periodicals, Inc. Comput Appl Eng Educ 16: 268–279, 2008; Published online in Wiley InterScience (www.interscience.wiley.com); DOI 10.1002/cae20148
Growth of SmNiO3 Thin Films on LaAlO3 Single Crystals
Authors: Ihzaz Nejib , Oumezzine Mohamed , Kreisel Jens , Vincent Henri , Pignard Stephane 
Published: June 2008

AbstractWe present experimental results on the growth of SmNiO3 epitaxial thin films, successfully deposited by a liquid source metal‐organic (MO) CVD technique. X‐ray diffraction (XRD) characterizations and wavelength dispersive spectroscopy (WDS) are performed in order to optimize the composition and the purity of the films. Depositions on Si (001) and LaAlO3 (001) substrates show that the SmNiO3 phase needs a perovskite substrate with a good lattice match in order to be epitaxially stabilized. Texture analysis performed on asymmetric diffraction lines reveals the epitaxial character of the growth; in‐plane and out‐of plane mosaicity are determined on a 1000 Å thick film.
Cyclometalation of Thiobenzophenones with Mononuclear Methyliron and ‐cobalt Complexes
Authors: Beck Robert , Sun Hongjian , Li Xiaoyan , Camadanli Sebnem , Klein Hans‐Friedrich 
Published: June 2008

AbstractUnder smooth conditions (–70 °C) thiobenzophenone derivatives react with [Fe(CH3)2(PMe3)4] to form five‐membered metallacycles 1 and 2 by C–H activation. These complexes show octahedral coordination geometry; with [Co(CH3)(PMe3)4], complexes 3 and 4 with trigonal‐bipyramidal coordination are formed. Reaction with basic [Ni(CH3)2(PMe3)3] causes reductive elimination (of ethane) with formation of zerovalent η2‐C=S complexes 5 and 6, possessing triangular‐planar coordination. The structures of the complexes were confirmed by X‐ray diffraction, and their coordination geometry is discussed.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
Cost–benefit analysis involving addictive goods: contingent valuation to estimate willingness‐to‐pay for smoking cessation
Authors: Weimer David L. , Vining Aidan R. , Thomas Randall K. 
Published: June 2008

AbstractThe valuation of changes in consumption of addictive goods resulting from policy interventions presents a challenge for cost–benefit analysts. Consumer surplus losses from reduced consumption of addictive goods that are measured relative to market demand schedules overestimate the social cost of cessation interventions. This article seeks to show that consumer surplus losses measured using a non‐addicted demand schedule provide a better assessment of social cost. Specifically, (1) it develops an addiction model that permits an estimate of the smoker's compensating variation for the elimination of addiction; (2) it employs a contingent valuation survey of current smokers to estimate their willingness‐to‐pay (WTP) for a treatment that would eliminate addiction; (3) it uses the estimate of WTP from the survey to calculate the fraction of consumer surplus that should be viewed as consumer value; and (4) it provides an estimate of this fraction. The exercise suggests that, as a tentative first and rough rule‐of‐thumb, only about 75% of the loss of the conventionally measured consumer surplus should be counted as social cost for policies that reduce the consumption of cigarettes. Additional research to estimate this important rule‐of‐thumb is desirable to address the various caveats relevant to this study. Copyright © 2008 John Wiley & Sons, Ltd.
The gut-brain-liver axis: A new option to treat obesity and diabetes?
Authors: Beraza Naiara 
Published: June 2008

Wang PY, Caspi L, Lam CK, Chari M, Li X, Light PE, et al. Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production. Nature 2008;452:1012–1016. www.nature.com (Reprinted with permission.)

Abstract
Energy and glucose homeostasis are regulated by food intake and liver glucose production, respectively. The upper intestine has a critical role in nutrient digestion and absorption. However, studies indicate that upper intestinal lipids inhibit food intake as well in rodents and humans by the activation of an intestine–brain axis. In parallel, a brain–liver axis has recently been proposed to detect blood lipids to inhibit glucose production in rodents. Thus, we tested the hypothesis that upper intestinal lipids activate an intestine–brain–liver neural axis to regulate glucose homeostasis. Here we demonstrate that direct administration of lipids into the upper intestine increased upper intestinal long-chain fatty acyl-coenzyme A (LCFA-CoA) levels and suppressed glucose production. Co-infusion of the acyl-CoA synthase inhibitor triacsin C or the anaesthetic tetracaine with duodenal lipids abolished the inhibition of glucose production, indicating that upper intestinal LCFA-CoAs regulate glucose production in the preabsorptive state. Subdiaphragmatic vagotomy or gut vagal deafferentation interrupts the neural connection between the gut and the brain, and blocks the ability of upper intestinal lipids to inhibit glucose production. Direct administration of the N-methyl-d-aspartate ion channel blocker MK-801 into the fourth ventricle or the nucleus of the solitary tract where gut sensory fibres terminate abolished the upper-intestinal-lipid-induced inhibition of glucose production. Finally, hepatic vagotomy negated the inhibitory effects of upper intestinal lipids on glucose production. These findings indicate that upper intestinal lipids activate an intestine–brain–liver neural axis to inhibit glucose production, and thereby reveal a previously unappreciated pathway that regulates glucose homeostasis.
Histological changes in HCV antibody–positive, HCV RNA–negative subjects suggest persistent virus infection
Authors: Hoare Matthew , Gelson William T. H. , Rushbrook Simon M. , Curran Martin D. , Woodall Tracy , Coleman Nicholas , Davies Susan E. , Alexander Graeme J. M. 
Published: June 2008

Abstract

It is unclear whether hepatitis C virus (HCV) has been eradicated or persists at a low level in HCV antibody–positive HCV RNA–negative individuals. The natural history and liver histology are not well characterized. One hundred seventy-two HCV antibody–positive, serum HCV RNA–negative patients underwent diagnostic liver biopsy between 1992 and 2000 and were followed a median 7 years (range, 5–12). Patients with any possible cause of liver injury other than HCV were excluded. A single histopathologist scored sections using Ishak criteria. Characterization of the inflammatory infiltrate in selected cases used a novel semiquantitative technique and compared with HCV RNA–positive patients and healthy controls. One hundred two patients were excluded because of a risk factor for liver injury other than HCV. Seventy patients met the study criteria; four (5.7%) became HCV RNA–positive during follow-up. Sixty-six cases remained HCV RNA–negative; five (7.5%) had a normal liver biopsy; 54 (82%) had fibrosis (stage 2 or 3 in 16 (24%)). Nonviremic cases revealed expanded portal tracts (

P

< 0.05), with fewer CD4+ (

P

< 0.05) and more CD8+ cells (

P

< 0.05) than healthy controls, but were indistinguishable from HCV RNA–positive cases for these parameters. Lobular CD4 staining, absent in healthy controls, was noted in both HCV RNA–negative and –positive cases and was more marked in the latter (

P

< 0.05) with a sinusoidal lining cell distribution.

Conclusion:

Nonviremic HCV antibody–positive patients have a liver biopsy that is usually abnormal. Fibrosis was present in most with similar inflammatory infiltrate to viremic cases. The presence of a CD8+ rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA–negative cases. (Hepatology 2008;48;1737-1745.)
Expression of matrix metalloproteinases in the neurogenic niche of the adult monkey hippocampus after ischemia
Authors: Lu Li , Tonchev Anton B. , Kaplamadzhiev Desislav B. , Boneva Nadezhda B. , Mori Yoshimi , Sahara Shunya , Ma Dexuan , Nakaya Masa‐aki , Kikuchi Mitsuru , Yamashima Tetsumori 
Published: June 2008

AbstractMatrix metalloproteinases (MMPs), zinc‐dependent endopeptidases capable of remodeling extracellular matrix and regulating cellular signals, have been implicated in various neurological functions and diseases. However, the role of MMPs in the adult neurogenesis still remains to be clarified, particularly in the primate. Here, we studied differential expression of MMP9/2 in the neurogenic niche of the hippocampal dentate gyrus (DG) after transient global brain ischemia in young adult macaque monkeys. Zymography demonstrated biphasic upregulation of MMP9 in acute (Days 1–3) and delayed (Days 7–15) phases of postischemic reaction, whereas the level of MMP2 was elevated only in the delayed phase. Immunofluorescence histochemistry showed that MMP9 and MMP2 colabeled with markers of endothelial cells, astrocytes, and newborn neurons in the subgranular zone (SGZ) of the DG, and also that the percentage of coexpression significantly increased in the delayed postischemic phase, as compared with controls. However, colabeling with different cell selective markers reached its peak at different time points, i.e., with endothelial cells on Day 7, whereas with astrocytes and newborn neurons on Day 15, respectively. MMPs were localized both in the perikarya and dendrites in the newborn neurons. In conclusion, MMP9/2 expression was regulated in a cell‐ and time‐specific manner in hippocampal neurogenic niche of adult primates. © 2008 Wiley‐Liss, Inc.