Mechanistic Differences (mechanistic + difference)

Distribution by Scientific Domains


Selected Abstracts


Enhanced reactivity in the ammonolysis of phenyl thiolacetates in aqueous medium

INTERNATIONAL JOURNAL OF CHEMICAL KINETICS, Issue 1 2002
D. Rajarathnam
The ammonolysis of several substituted phenyl thiolacetates is kinetically studied in aqueous medium, 18°C, ionic strength 0.1 M (KCl). By following the leaving groups spectrophotometrically (,max = 260,410 nm), under excess free ammonia, pseudo-first-order rate coefficients (kobs) are obtained. The plots of (kobs , kH) against free ammonia concentration are linear at constant pH. The macroscopic nucleophilic substitution rate coefficients (kN) are obtained as the slopes of these plots and found to be pH-independent for all the thiolesters. The Brönsted-type plot (log kN against pKa of leaving groups) and the Hammett plot (log kN against , values of substituents) obtained for the title reactions of thiolesters are linear with slope values of ,lg = ,0.34 and , = 0.74 respectively. From the magnitude of these values, experimental data, the kinetic law, and the analysis of products, it is deduced that the ammonolysis of thiolesters proceeds through a simple bimolecular nucleophilic substitution pathway with a zwitterionic tetrahedral addition intermediate (T±), whereby its formation is rate-determining (k1 step). Comparison of this reaction of thiolesters with a similar reaction of analogue oxyesters shows a mechanistic difference. Further, for thiolesters there is a rate enhancement with larger kN values. The change in mechanism and enhanced reactivity observed by substitution of the oxygen atom by sulphur atom on the phenyl moiety are discussed in detail. © 2001 John Wiley & Sons, Inc. Int J Chem Kinet 34: 18,26, 2002 [source]


Expression of p53 in lesions and unaffected skin of patients with plaque-type and guttate psoriasis: A quantitative comparative study

THE JOURNAL OF DERMATOLOGY, Issue 6 2007
Ayça Cordan YAZICI
ABSTRACT Psoriasis is a common inflammatory and hyperproliferative skin disease characterized by hyperproliferation of keratinocytes. The pathogenesis of psoriasis has yet to be determined. The control of cell growth is a delicately balanced process, regulated by external signals or the internal genetic program of an individual cell. In psoriasis, these processes are disturbed and some candidate genes like p53 are suspected of being involved in the pathogenesis of the disease. The p53 protein is essential for the regulation of cell proliferation. The study was performed on 32 patients with psoriasis (24 plaque type, eight guttate type). Biopsy specimens for immunohistochemical determination of p53 protein expression were collected from both the lesional and the nonlesional skin sites that were not exposed to sun in all of the patients (n = 32). Taking the ultraviolet (UV) exposure of the skin into consideration, a third skin sample was taken from each patient (n = 7) who had lesions on the sun-exposed areas. Immunohistochemical assessment of p53 expression in skin was determined as p53 protein expression per 1000 cells (keratinocytes). The statistical analysis revealed that the expressions of p53 per 1000 cells were higher in non-sun-exposed lesional skin than the non-sun-exposed nonlesional skin, also in plaque-type psoriasis than guttate-type psoriasis (P = 0.000, P = 0.046, P = 0.037, respectively). There was a positive correlation between the p53 expression in non-sun-exposed lesional skin versus expression in sun-exposed lesional skin (cubic centimeters = 0.811, P = 0.027). Our results show a stronger association of elevated p53 expression with chronic rather than acute inflammatory psoriasis. This may indicate a mechanistic difference between plaque-type and guttate psoriasis. Alternatively, this could reflect a chronological course as the disease transitions from an acute to a chronic phase. [source]


Syntactic Priming Effects in Comprehension: A Critical Review

LINGUISTICS & LANGUAGE COMPASS (ELECTRONIC), Issue 10 2010
Kristen M. Tooley
Syntactic priming occurs when processing of a target sentence is facilitated following processing of a prime sentence that has the same syntactic structure (Bock, 1986 Cognitive Psychology, 18. 355,387). Syntactic priming has been widely investigated in production (Bock, 1986 Cognitive Psychology, 18. 355,387; Bock and Griffin, 2000 General. 129(2). 177,192; Cleland and Pickering, 2003. Journal of Memory and Language, 49. 214,230; Cleland and Pickering 2006. Journal of Memory and Language, 54. 185,198; Pickering and Branigan, 1998. Journal of Memory and Language, 39. 633,651; and others), but only relatively recently in comprehension (Arai et al. 2007. Cognitive Psychology, 54(3). 218,250; Ledoux et al., 2007. Psychological Science. 18(2). 135,143; and others). This article reviews the current literature on syntactic priming in comprehension and contrasts these findings to those in production. Critically, syntactic priming effects in comprehension are observed more often when prime and target sentences share a content word, whereas in production, these effects are often observed when there are no shared content words between the primes and targets. Possible explanations for the differing degrees of lexical dependency between syntactic priming effects in production and in comprehension are posed and include differences in task paradigms and stimuli, differences in time course and syntactic processing between the two modalities, and mechanistic differences. Implications from the reviewed literature are then considered in attempts at determining the most likely mechanistic explanation for syntactic priming effects in both comprehension and production. A residual activation account (Pickering and Branigan, 1998. Journal of Memory and Language, 39. 633,651), an implicit learning account (Bock and Griffin, 2000 General. 129(2). 177,192; Chang et al. 2006. Psychological Review, 113(2). 234,272), and a dual mechanism account (Tooley, 2009. Is Syntactic Priming in Sentence Comprehension Really Just Implicit Learning? Paper presented to the 22nd Annual CUNY Conference on Human Sentence Processing, Davis, March 26,28) are outlined. The dual mechanism account may prove more consistent with a wider range of the reviewed research findings. [source]


Different effects of cardiac versus skeletal muscle regulatory proteins on in vitro measures of actin filament speed and force

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Emilie Warner Clemmens
Mammalian cardiac and skeletal muscle express unique isoforms of the thin filament regulatory proteins, troponin (Tn) and tropomyosin (Tm), and the significance of these different isoforms in thin filament regulation has not been clearly identified. Both in vitro and skinned cellular studies investigating the mechanism of thin filament regulation in striated muscle have often used heterogeneous mixtures of Tn, Tm and myosin isoforms, and variability in reported results might be explained by different combinations of these proteins. Here we used in vitro motility and force (microneedle) assays to investigate the influence of cardiac versus skeletal Tn and Tm isoforms on actin,heavy meromyosin (HMM) mechanics. When interacting with skeletal HMM, thin filaments reconstituted with cardiac Tn/Tm or skeletal Tn/Tm exhibited similar speed,calcium relationships and significantly increased maximum speed and force per filament length (F/l) at pCa 5 (versus unregulated actin filaments). However, augmentation of F/l was greater with skeletal regulatory proteins. Reconstitution of thin filaments with the heterogeneous combination of skeletal Tn and cardiac Tm decreased sliding speeds at all [Ca2+] relative to thin filaments with skeletal Tn/Tm. Finally, for filaments reconstituted with any heterogeneous mix of Tn and Tm isoforms, force was not potentiated over that of unregulated actin filaments. Combined the results suggest (1) that cardiac regulatory proteins limit the allosteric enhancement of force, and (2) that Tn and Tm isoform homogeneity is important when studying Ca2+ regulation of crossbridge binding and kinetics as well as mechanistic differences between cardiac and skeletal muscle. [source]


Disturbed morphogenesis of cardiac outflow tract and increased rate of aortic arch anomalies in the offspring of diabetic rats

BIRTH DEFECTS RESEARCH, Issue 12 2004
Daniël G.M. Molin
Abstract BACKGROUND Maternal diabetes (MD) is a risk factor for offspring to develop cardiovascular anomalies; this is of growing clinical concern since the number of women in childbearing age with compromised glucose homeostasis is increasing. Hyperglycemia abrogates cardiovascular development in vitro; however, a link to cardiovascular defects in diabetic offspring remains to be investigated. METHODS We have studied cardiovascular development in offspring of MD rats by examining serial histological sections of GD 12.0,18.0 offspring. Development of pharyngeal arch artery malformations was analyzed and related to intracardiac anomalies. RESULTS Pharyngeal arch artery and intracardiac defects were present in 27 of 37 MD GD 13.0,18.0 offspring. Early sixth arch arteries showed abrogated arteriogenesis, whereas fourth arch artery defects developed as a result of abnormal remodeling. Morphometrical analysis showed increased apoptosis in regressing artery segments and reduced apoptosis in persisting artery segments. Double outlet right ventricle with infundibular stenosis (tetralogy of Fallot) was predominantly found in combination with sixth artery defects and pulmonary atresia. As confirmed by morphometric analysis and three-dimensional (3D)-reconstructions, outflow tract defects coincided with endocardial cushion hypoplasia. Cases with teratology of Fallot additionally showed a shorter outflow tract. No relation with apoptosis or disturbed neural crest cell migration was found. CONCLUSIONS Our data uniquely demonstrate mechanistic differences involved in the development of sixth and fourth artery anomalies. Whereas increased apoptosis induces fourth artery anomalies, pulmonary outflow obstruction abrogates sixth artery differentiation independent of apoptosis. The model presented allows analysis of diabetic conditions on cardiovascular development in vivo, essential for elucidating this teratology. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]