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Additive Fashion (additive + fashion)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Integration of motion parallax with binocular disparity specifying different surface shapes

JAPANESE PSYCHOLOGICAL RESEARCH, Issue 1 2002
Makoto Ichikawa
Abstract: We investigated the interaction between motion parallax and binocular disparity cues in the perception of surface shape and depth magnitude by the use of the random dot stimuli in which these cues specified sinusoidal depth surfaces undulating with different spatial frequencies. When ambiguous motion parallax is inconsistent with unambiguous disparity cue, the reasonable solution for the visual system is to convert the motion signal to the flow on the surface specified by disparity. Two experiments, however, found that the visual system did not always use this reasonable solution; observers often perceived the surface specified by a composite of the two cues, or the surface specified by parallax alone. In the perception of this composite of the two cues, the apparent depth magnitude increased with the increase of the depth magnitude specified by both cues. This indicates that the visual system can combine the depth magnitude information from parallax and disparity in an additive fashion. The interference with parallax by disparity implies that the parallax processing is not independent of the disparity processing. [source]

Ethanol-Responsive Genes (Crtam, Zbtb16, and Mobp) Located in the Alcohol-QTL Region of Chromosome 9 Are Associated With Alcohol Preference in Mice

ALCOHOLISM, Issue 8 2009
Julia Weng
Background:, Previously, our group identified cytotoxic and regulatory T-cell molecule (Crtam), zinc finger and BTB domain containing 16 (Zbtb16), and myelin-associated oligodendrocytic basic protein (Mobp) as ethanol-responsive genes in the mouse brain by gene expression profiling. In this study, we used a genetic co-segregation analysis to assess the association of Crtam, Zbtb16, and Mobp with the alcohol preference (AP) phenotype in the alcohol-preferring C57BL/6J (B6) and alcohol avoiding DBA/2J (D2) strains of mice. Methods:, Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to confirm previous microarray analysis results that Crtam, Zbtb16, and Mobp brain mRNA levels in the B6 and D2 strains are altered by ethanol treatment. The association of the 3 genes with AP was assessed in a F2 population (n = 427) derived from the reciprocal crosses involving the B6 and D2 strains. Each F2 individual was assessed for their AP using the 2 bottle choice test and genotyped for Crtam, Zbtb16, and Mobp single nucleotide polymorphisms (SNPs) that differ between B6 and D2 mice. Results:, Semi-quantitative RT-PCR analysis confirmed that Crtam, Zbtb16, and Mobp are ethanol-responsive genes. The SNP analyses show that alleles of the 3 genes co-segregate with the AP phenotype in F2 mice, where individuals homozygous for the B6 allele have higher AP than those homozygous for the D2 allele. Also, the Crtam,Zbtb16 loci that are tightly linked and the Mobp locus act in an additive fashion in determining the relative AP phenotype. Conclusion:, Our results are consistent with the hypothesis that Crtam, Zbtb16, and Mobp may be involved in AP in mice. The nature of this association remains to be established and may reflect a direct effect of these genes or an indirect effect caused by linked genes on mouse chromosome 9. [source]

Genetic analysis of pancreatic duct hyperplasia in Otsuka Long,Evans Tokushima Fatty rats: Possible association with a region on rat chromosome 14 that includes the disrupted cholecystokinin-A receptor gene

PATHOLOGY INTERNATIONAL, Issue 3 2001
Naohide Kanemoto
An Otsuka Long,Evans Tokushima Fatty (OLETF) strain of rat spontaneously developed hyperglycemia, hyperinsulinemia, insulin resistance and mild obesity, which had been studied as animal model for type II diabetes mellitus (T2DM). Recently, we observed that this strain coincidentally developed atypical hyperplasia of the choledocho-pancreatic ductal epithelium with a complete incidence. In an effort to locate genes responsible for this hyperplasia, we prepared 288 backcross progeny from a mating between OLETF rats and BN rats (which do not develop hyperplasia), and performed a genome-wide scan using 207 polymorphic genetic markers. We observed a prominent association of hyperplasia with a region involving a marker locus D14Mit4 (P = 0.00020, Fisher's exact test) and Cckar (the cholecystokinin-A receptor gene; P = 0.00025, Fisher's exact test) which is known to be disrupted in an OLETF strain. Our findings indicated that epithelial hyperplasia of the choledocho-pancreatic duct is associated with a region on rat chromosome 14 around the Cckar gene in an additive fashion with another two susceptible loci, each on chromosome 9 and 7. This implied the possibility that Cckar deficiency could result in a predisposition towards pancreatic duct hyperplasia. [source]

High tolerance to simultaneous active-site mutations in TEM-1 ,-lactamase: Distinct mutational paths provide more generalized ,-lactam recognition

PROTEIN SCIENCE, Issue 1 2009
Pierre-Yves De Wals
Abstract The diversity in substrate recognition spectra exhibited by various ,-lactamases can result from one or a few mutations in the active-site area. Using Escherichia coli TEM-1 ,-lactamase as a template that efficiently hydrolyses penicillins, we performed site-saturation mutagenesis simultaneously on two opposite faces of the active-site cavity. Residues 104 and 105 as well as 238, 240, and 244 were targeted to verify their combinatorial effects on substrate specificity and enzyme activity and to probe for cooperativity between these residues. Selection for hydrolysis of an extended-spectrum cephalosporin, cefotaxime (CTX), led to the identification of a variety of novel mutational combinations. In vivo survival assays and in vitro characterization demonstrated a general tendency toward increased CTX and decreased penicillin resistance. Although selection was undertaken with CTX, productive binding (KM) was improved for all substrates tested, including benzylpenicillin for which catalytic turnover (kcat) was reduced. This indicates broadened substrate specificity, resulting in more generalized (or less specialized) variants. In most variants, the G238S mutation largely accounted for the observed properties, with additional mutations acting in an additive fashion to enhance these properties. However, the most efficient variant did not harbor the mutation G238S but combined two neighboring mutations that acted synergistically, also providing a catalytic generalization. Our exploration of concurrent mutations illustrates the high tolerance of the TEM-1 active site to multiple simultaneous mutations and reveals two distinct mutational paths to substrate spectrum diversification. [source]